CLASSIFICATION OF MEDICAL
PARASITOLOGY
Parasites of medical importance come under
the kingdom called animalia, Includes the
microscopic single-celled eukaroytes known
as
protozoa.Incontrast,helminthes
are
macroscopic, multicellular worms possessing
well differentiated tissues and complex organs
belonging to the kingdom animalia.
1
Lecture One
• MedicalParasitology is generally classifiedinto:
• Medical Protozoology - Deals with the study
of medically important protozoa.
• Medical Helminthology - Deals with the study
of helminthes (worms) that affect man.
• Medical Entomology - Deals with the study of
arthropods which cause or transmit disease to
man.
2
Lecture One
Classification of Medically important
Parasites
The parasite divide into three main groups
Protozoa
Parasite consist of a
single celled organism
which is morphologically
and functionally
complete and can
perform all function of
life ,reproduction by
asexual or sexual
3
Metazoa
Parasite consiste of
multicellular celles,
Bilaterally
symmetrical
animals,having welldifferentiated tissues
and complex organ
Lecture One
Arthropoda(Medic
Entomology) al
include
Insecta (Butter fly)
Arachnida (Mite)
Crustacea (Cyclops)
Taxonomic classification of Protozoa
Sub kingdom
Protozoa
4
Phylum
Class
Genusexamples
Speciesexamples
Sarcodina(Amoeba)
move by
pseudopodia
Entamoeba
Endolimax
Iodameba
Dientameba
E. hstolytica
E.nana
I.butchlii
D.fragilis
Mastigophora
(Flagellates)
move by flagella
Giardia
Trichmonas
Trypanosoma
Leishmania
G. Lamblia
T.vaginalis
T.brucci
L.donovani
Apicomplexa
(Sporozoa)
no organelle of
Locomotion
Plasmodium
Toxoplasma
P. falciparum
T.gonidi
C.parvum
I.beli
Ciliophora
move by cillia
Balantidium
Sarcomastigophora
further divided into
Cryptosporidium
Isospora
Lecture One
B. coli
Important pathogenic protozoa and commonly caused
diseases.
Type and location
Species Disease
Species
Disease
Intestinal tract
Entamoeba histolytica
Giardia lamblia
Cryptosporidium parvum
Balantidium coli
Isospora belli
Cyclospora cayentanensis
Ambiasis
Giardiasis
Cryptosporidiosis
Balantidiasis
Isosporiosis
Cyclosporiasis
Urogenital tract
Trichomonas vaginalis
Trichomoniasis
Blood and tissue
Plasmodium species
Toxoplasma gondii
Trypanasoma species
Leishmania species
Naegleria species
Acanthamoeba species
Babesia microti
Malaria
Toxoplasmosis
Trypanosomiasis
Leishmaniasis
Amoebic Meningoencephalitis
Amoebic Meningoencephalitis
Babesiosis
5
Lecture One
The Protozoa
General:
• There are about 45,000 protozoan species;
around 8000 are parasitic, and around 250
species are important to humans.
• Diagnosis - must learn to differentiate between
the harmless and the medically important. This is
most often based upon the morphology of
respective organisms.
• Transmission - mostly person-to-person, via
fecal-oral route; fecally contaminated food or
water; other means include sexual transmission,
insect bites or insect feces.
6
Lecture One
The Protozoa
Diagnostic Features:
• Nuclear structure - important in species differentiation.
• Size - helpful in identifying organisms; must have
calibrated objectives on the microscope in order to
measure accurately.
• Cytoplasmic inclusions - chromatoid bars (coalesced
RNA); red blood cells; food vacuoles containing
bacteria, yeast, etc.
• Appearance of cytoplasm - smooth & clean or
vacuolated.
• Type of motility - directional or non-directional; sluggish
or fast.
7
Lecture One
The Protozoa
Nuclear Structure:
• Chromatin - nuclear DNA. Present as “peripheral”
chromatin and the karyosome.
• Karyosome - a small mass of chromatin within the
nuclear space. Also called “endosome” or
“centrosome.”
• Peripheral Chromatin - chromatin adhering to the
nuclear membrane.
• Nuclear membrane - membrane surrounding all
nuclear material.
Chromatoid body or “bar” - coalesced RNA within the
cytoplasm of the cyst stage.
8
Lecture One
The Protozoa
General:
• Trophozoite - the motile vegetative
stage; multiplies via binary fission;
colonizes host.
• Cyst - the inactive, non-motile, infective
stage; survives the environment due to
the presence of a cyst wall. Cysts do
not multiply, however, some organisms
divide within the cyst wall.
9
Lecture One
They are three groups of Amoeba
Pathogenic :E. histolytica
10
Nonpathogenic ;Entamoeba coli
E.gingivalis
Endolimax nana
Iodameba butschili
Dientameba fragilis
Lecture One
Free Living
Neagleria fowleria
Pathogenic Amoeba
Entamoeba histolytica
• INTRODUCTION
• Amoebas primitive unicellular microorganisms with a
relatively simple life cycle which
• can be divided into two stages:
• Trophozoite : actively motile feeding stage
• Cyst : quiescent,resistanse ,infective stage
• The reproduction is through binary fission
• Motility by extention of pseudopodia (False Feet)
11
Lecture One
Trophozoite :Viable trophozoites vary in size from
about 10-60μm in diameter.
Motility is rapid,progressive, and
unidirectional,through pseudopods.
The nucleus is characterized by
evenly arranged chromatin on the
nuclear membrane and the
presence of a small,compact,
centrally located karyosome. The
cytoplasm is usually described as
finely granular with few ingested
bacteria or debris in vacuoles. In the
case of dysentery,however, RBCs
may be visible in the cytoplasm, and
this
feature
is
diagnostic
forE.histolytica.
12
Lecture One
Cyst : (infectivestage)
• Cysts range in size from 1020μm.
contains
four
nuclei when mature The
immature
cyst
has
inclusions
namely;
glycogen
• mass and chromatoidal
bars. As the cyst matures,
the glycogen completely
disappears;
• the chromotiodials may
also be absent in the
mature cyst..
13
Lecture One
Life cycle of E. histolytica
Infection by E. histolytica occures by ingestion of cyst in fecally
contaminated food,water or hands,the cyst resistane to the
gastric environmentand passes to small intestine where it
excystation Trophozoite are released which migrate to large
intestine ,the troph. Multiply by binary fission and produce cyst
(Mature or immature) which are passed in feces, (trophozoite
can be passed in diarrheal stool,but rapidly destroyed outside
the body,the troph.remain confined to the intestinal lumen , in
some individuals troph. non invade the intestinal who are thus
asymptomatic carriers but in other patient troph. Invade the
intestinal
submucosa
causes
intestinal
disease
(lesion,Ulcer,Flaske shape ) or Invasion of blood vessels leads
to secondary extra intestinal lesions.May be invade liver, lung
and brain.the cyst can survive days to weeks in the external
environment and are responsible for transmission.
14
Lecture One
life cycle of E.histolytica
15
Lecture One
Epidemiology
E.histolytica has a worldwide distribution. Although it is
found in cold areas, theincidence is highest in tropical and
subtropical regions that have poor sanitation and
contaminated water. About 90% of infections are
asymptomatic, and the remaining produces a spectrum of
clinical syndrome. Patients infected withE.hisolytica pass
non infectious trophozotes and infectious cysts in their
stools. Therefore, the main source of water and food
contamination is the symptomatic carrier who passes
cysts.
Symptomatic amebiasis is usually sporadic. The epidemic
form is a result of direct person-to-person faecal-oral
spread under conditions of poor personal hygiene
16
Lecture One
Pathogenesis
Trophozoites divide and produce extensive
local necrosis in the large intestine. Invasion
into the deeper mucosa with extension into
the peritoneal cavity may occur. This canlead
to secondary involvement of other organs,
primarily the liver but also the lungs,brain,
and heart. Extraintestinal amebiasis is
associatedwithtrophozoites. Amoebasmultiply
rapidly in an anaerobic environment, because
the trophozites are killed by ambient oxygen
concentration.
17
Lecture One
Clinical features
The outcome of infection may result in a carrier state,
intestinal amebiasis, or exteraintestinal amebiasis.
Diarrhoea, flatulence, and cramping are complaints of
symptomatic patients. More severe disease is
characterised by the passing ofnumerous bloody stools in
a day. Systemic signs of infection (fever, leukocytosis,
rigors)are present in patients with extraintestinal
amebiasis. The liver is primarily involved,because
trophozoites in the blood are removed from the blood by
the portal veins. Theright lobe is most commonly
involved, thus pain over the liver with hepatomegaly and
elevation of the diaphragm is observed.
18
Lecture One
Laboratory diagnosis
In intestinal amoebiasis:
• Examination of a fresh dysenteric faecal specimen or rectal
scraping fortrophozoite stage. (Motile amoebae containing red
cells are diagnostic of amoebicdysentery).
• Examination of formed or semiformed faeces for cyst stage.
(Cysts indicateinfection with either a pathogenic E.histolytica or
non-pathogenic E.dispar.)
Extraintestinal amoebiasis
• Diagnosed by the use of scanning procedures for liver and
other organs.
• Specific serologic tests, together with microscopic
examination of the abscess material, can confirm the diagnosis.
19
Lecture One
Treatment
Acute, fulminating amebiasis is treated with
metrondiazole
followed
by
iodoquinol,
andasymptomatic carriage can be eradicated with
iodoquinol, diloxanide furoate, or paromomycin. The
cysticidal agents are commonly recommended for
asymptomaticcarriers who handle food for public
use,Metronidazole, chloroquine, and diloxanide
furoate can be used for the treatment ofextra
intestinal amoebiasis.
20
Lecture One
OTHER AMEBAE INHABITING THE ALIMENTARY CANAL
Entamoeba coli
the life cycle stages include; trophozoite, precyst, cyst, metacyst, and
metacystic trophozoite. Typically the movements of trophozoites are
sluggish, withbroad short pseudopodia and little locomotion, but at a
focus the living specimen cannot be distinguished from the active
trophotozoite of E.histolytica. However, the cysts are remarkably
variable in size. Entamoeba coli is transmitted in its viable cystic stage
through faecal contamination. Ε.coli as a lumen parasite is nonpathogenic and produces no symptoms. The mature cyst (with more
than four nuclei) is the distinctive stage to differentiate E.coli from the
pathogenic E.histolytica. Specific treatment is not indicated since this
amoeba is non-pathogenic. The presence of E.coli in stoolspecimen is
evidence for faecal contamination. Prevention depends on better
personal hygiene and sanitary disposal of human excreta.
21
Lecture One
E. histolytica Troph.( 18 – 60 µm )
The motile in saline, active progressive and directional
E. Coli Troph. ( 20 – 50 µm )
The motile in saline sluggish rarely progressive not directional
22
Lecture One
Table : Differentiation of trophozoite and cyst of E. histolytica and E. coli
Note : as E. coli is more commonly found in the dysenteric stool, the
morphological differences from the pathogenic species E. histolytica is
shown in the table below
Entamoeba histolytica
Trophozoiti.
Size :
Motility :
Cytoplasm :
Cytoplasmic
inclusions :
Nucleus :
Stained with iodine :
Nuclear character :
23
20 to 30µm.
Very active
Clearly defined into ectoplasm
and endoplasm.
In food vacuoles, Red blood
cells, leucocytes and tissue
debris but no bacteria
Not visible in unstained
preparation .
Central karyosome; fine
chromatin granules line the
delicate nuclear membrane .
Lecture One
Entamoeba coli
20 to 40 µm.
Sluggish
Not defined; ectoplasm .
Bacteria and other materials but
never red blood cells .
visible in unstained preparation .
Eccentric karyosome; coarse
chromatin granules line the thick
nuclear membrane .
Entamoeba histolytica
cyst :
Stained with iodine :
Size :
Nucleus :
Glycogen mass :
6 to 15 µm.
1 to 4 central karyosome.
Visible in uninucleate stage .
Chromatoid bodies :
Rounded bars .
E. histolytica Cyst ( 5 – 20 µm )
24
Lecture One
Entamoeba coli
15 to 20 µm.
1 to 8 eccentric karyosome .
Large and visible in the binucleate stage.
Filamentous, thread – like with square or
pointed ends .
E. Coli Cyst ( 15 – 33 µm )
Entamoeba hartmanni (non pathogenic)
In all of its life–cycle stage, E.hartmanni resembles
E.histolytica except in size, yet there is a slight overlap in
the size range. The trophozoites do not ingest red blood
cells, and their motility is generally less vigorous than
that of E.histolytica. As in other amebae, infection is
acquired by ingestion of food or water contaminated
with cyst-bearing faeces. Identification is based on
examination of small amebae in unstained or iodinestained preparations. Usually no treatment is
indicated,measures generally effective against faecalborne infections will control this amoebic infection
25
Lecture One
Entamoeba polecki
a relatively cosmopolitan parasite of hog and
monkey. It can cause human disease but is
rarely isolated. The disease is manifested as
mild, transientdiarrhoea. The diagnosis of
E.polecki infection is confirmed by the
microscopic detection of cysts in stool
specimens. Treatment is the same as for
E.histolyticainfection. Prevention is achieved
by good personal hygiene.
26
Lecture One
Endolimax nana
Is a lumen dweller in the large intestine, primarily at the
cecal level,where it feeds on bacteria. The life cycle is
similar to E.histolytica. Motility is typically sluggish.
Human infection results from ingestion of viable cysts in
polluted water or contaminated food. Typical ovoid cysts
of E.nana are confirmative. Rounded cysts and living
trophozoites are often confused with E.hartmanni and
E.histolytica. No treatment is indicated for this
nonpathogenicinfection. Prevention can be achieved
through personal cleanliness and community sanitation.
27
Lecture One
Endolimax nana
• live in large intastine
smallest amoeba
•Life cycle is similar to
E.histolytica
•Troph.has large
karyosome
•Feed on bacteria
Cyst is small in size ,oval or
spherical in shape contain
four nuclei
28
Lecture One
Iodamoeba buetschlii: the natural habitat is the lumen of the large intestine, the
principal site probably being the caecum. The trophozoite
feeds on enteric bacteria; it is a natural parasite of man and
lower primates. It is generally regarded as a nonpathogenic
lumen parasite. No treatment is ordinarily indicated.
Prevention is based ongood personal hygiene and sanitation in
the community.
29
Lecture One
Entamoeba gingivalis
only the trophozoite stage presents,all species oral and
encystation probably does not occur. E.gingivalis is a
commensal, living primarily on exudate from the
margins of the gums, and thrives best on unhealthy
gums. No specific treatment is indicated. However the
presence of E.giingivalis suggests a need for better oral
hygiene.
30
Lecture One
Blastocystis hominis
is an inhabitant of the human intestinal tract previously
regarded as non-pathogenic . Its pathogenecity remains
controversial. The organism is found in stool specimen from
asymptomatic people as well as from people with persistent
diarrhoea. B.hominis is capable of pseudopodia extension and
retraction, and reproduces by binary fission or sporulation. The
classic form that is usually seen in the human stool specimen
varies tremendously in size, from 6-40μm. There are thin –walled
cysts involved in autoinfection, and thick–walled cysts
responsible for external transmission via the faecal-oral route.
The presence of large numbers of these parasites(five or more
per oil immersion microscopic field) in the absence of other
intestinal pathogens indicates disease. Treatment with
iodoquinol or metronidazole has been successful .
31
Lecture One
FREE-LIVING AMOEBAE
Among the numerous free-living amoebae of soil and
water
habitats, certain species of Naegleria,
Acanthamoeba and Balamuthia are facultative parasites
of man. Most human infections of these amoebae are
acquired by exposure to contaminated waterwhile
swimming. Inhalation of cysts from dust may account
for some infections.
32
Lecture One