GENERAL INTRODUCTION

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TERMS EMPLOYED IN PARASITOLOGY

• Parasite : living organism which receives

nourishment & shelter from another
organism where it lives.

• Host : an organism which harbours the

parasite.

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 TERMS EMPLOYED IN PARASITOLOGY
• Association of living things which live
together
– Symbiosis. An association in which hoth are so
dependent.upon each other that one cannot live
without the other. None of them suffers any harm.
– Commensalism. An association in which the
parasite only is deriving benefit without causing injury
to its host.
– Parasitism. An association in which the parasite
derives benefit & the host gets nothing in return but
always suffers some injury. The host, at the same
time, offers some resistance to the injury done by the
parasite and there may be some adaptation between
the parasite and the host.
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TERMS EMPLOYED IN PARASITOLOGY

• Zoonosis : evolution of a human disease

naturally acquired from an infection
primarily confined to vertebrate animals.

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 CLASSES OF PARASITES
• Ecto-parasite (Ectozoa)
– Lives outside on the surface of the body of the
host.

• Endo-parasite (Entozoa)
– Lives inside the body of the host: in the blood,
tissues, body cavities, digestive tract and
other organs.

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 CLASSES OF PARASITES
• Temporary Parasite
– Visits its host for a short period.

• Permanent Parasite
– Leads a parasitic life throughout the whole
period of its life.

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 CLASSES OF PARASITES
• Facultative Parasite
– Lives a parasitic life when opportunity arises.

• Obligatory Parasite
– Cannot exist without a parasitic life.

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 CLASSES OF PARASITES
• Occasional or Accidental Parasite
– Attacks an unusual host.

• Wandering or Aberrant Parasite

– Happens to reach a place where it cannot
live.

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 CLASSES OF HOSTS
• Definitive Host
– Either harbours the adult stage of the parasite
or where the parasite utilises the sexual
method of reproduction.

• Intermediate Host
– Harbours the larval stages of the parasite. In
some cases larval developments are
completed in two different intermediate hosts
which are then referred to as first and second
intermediate hosts respectively.
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 SCHEME FOLLOWED IN
PARASITOLOGICAL STUDY
• Phylum Protozoa
– Medical Protozoology.
• Phylum Platyhelminthes & Phylum
Nemathelminthes
– Medical Helminthology.
• Phylum Arthropoda
– Medical Entomology.

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 Superclass Superfamily
↓ ↓
Phylum  Subphylum  Class  Order  Family  Genus  Species
↑ ↑ ↑
Subclass Suborder Subfamily

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The study of animal parasites infecting man
and producing clinical manifestations
should include the following:
• History of the discovery of the parasite.
• Geographical distribution.
• Habitat inside the human host.
• Morphology and life cycle (staining
methods and cultivation).
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• Modes of infection: Reservoir host,
sources of infection, portal of entry, vehicle
of transmission.
• Effect of the parasite: Pathogenic lesions,
Clinical manifestations.
• Immunological responses.
• Methods for specific diagnosis.

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• Approved therapy for eradication of the
parasitic infection.
• Prophylactic measures for the prevention
of parasitic infection of the individual as
well as of the community.

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BLOOD AND TISSUE
FLAGELLATES

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 Structural pattern
• Body
• Nucleus
• Kinetoplast
• Flagellum
• Undulating membrane

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 Developmental stage
• Amastigote : rounded form without any external flagellum.
• Promastigote : form with kinetoplast lying anterior to the nucleus, the
flagellum arising near it emerges from the anterior end of the body.
• Opisthomastigote : form with kinetoplast lying posterior to the nucleus, the
flagellum arising near it, then pass through the body and emerges from the
anterior end.
• Epimastigote : form with kinetoplast lying anterior and close to the nucleus,
the flagellum arising near it emerges from side of the body to run along a
shorth undulating membrane.
• Trypomastigote : form with postnuclear kinetoplast situated at the posterior
end of the body, the flagellum arising near it emerges from side of the body
to run along a long undulating membrane.
• Choenomastigote : a new term for the peculiar ‘barley-corn form’, usually
with kinetoplast lying at the anterior end of the body, the flagellum arising
near it emerges at the anterior end of the body through a wide funnel-
shaped reservoir.

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TRYPANOSOMA

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 Classification
• Phylum : Protozoa
• Class : Mastigophora
• Order : Protomonadida
• Family : Trypanosomatidae
• Genus : Trypanosoma
• Species :
– Trypanosoma brusei gambiense
– Trypanosoma brucei rhodisiense
– Trypanosoma cruzi
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 Morphology
• Minute, actively motile, fusiform, flattened from
side to side
• Long, sinous body : tapering anterior, blunt
posterior end
• Flagellum
– 5-9 striated parallel microtubules in a cytoplasmic
sheath
– Project from anterior end after passing along margin
of undulating membrane
• Undulating membrane
– Wavy fold of the periplast on the convex border
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 Morphology
• Nucleus
– Large oval
– Central karyosome
• Kinetoplast : compact array of DNA fibrils
in the mitochondrial matrix
• Cytoplasm : refractile volutin granules,
vacuoles
• Wavy spiral motion
• Reproduction : binary longitudinal fission
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Figure 1. Developmental form of Tripanosomatidae

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Trypanosoma brucei
gambiense

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 Disease
• Gambian trypanosomiasis
• Mid-African sleeping sickness

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 Morphology
• In blood
– Polymorphic
• Typical long
• Slender trypanosomes
• Short, stumpy forms
• Size : length 15-35 µ, width 1.5-4.0 µ

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 26
Figure 2. Life cycle of Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense
 Epidemiology
• Limited to tropical West & Central Africa
• Limited to range of its vectors
– The palpalis group of tsetse flies
• Endemic area
– Incidence < 1% in
– Precentage of infected flies 2-4%
• Seasonal incidence
– Distribution & prevalence of insect vector
– Humidity & temperature (optimal 24-30ºC)
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 Epidemiology
• Transmitted to human
– Bite of infected tsetse fly
– Mechanical transmision
– Coitus
– Congenital : rare

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 Pathology & Symptomatology
• Severity
– Mild type
– Severe fulminating type
• Incubation period : 14 days – delayed for
months

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 Pathology & Symptomatology
• Typical case
– Acute stage : during first year
• Trypanosomes multiplying in blood & lymphatics
• Iregular fever, headache, joint & muscle pain, rash
• Enlarge of superficial lymphnodes
– Chronic stage ; second year
• Central nervous system change
• Ischemic softening tissue, ptechial hemorrhages
– Terminal sleeping stage : second or third year
• Gradually more & more difficult to rouse

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 Diagnosis
• Suspected
– From endemic area
– Acute infection
• Irregular fever & palpable lymphnodes
• Definite laboratory diagnosis
– Finding trypanosomes in blood, lymphnode,
bone marrow, cerebrospinal
• Presumtive diagnosis
– Increasing IgM in cerebrospinal fluid & serum

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 Treatment
• Early infection
– Pentamidine isethionate 4 mg/kg/day im (10 days)
– Suramin sodium 100-200 mg test dose iv, 1 g iv on
day 1,3,7,14,21
• Late infection
– Melarsoprol 2-3,6 mg/kg/day iv 3 doses; afte 1 week
3,6 mg/kg/day iv 3 doses
• May be repeated after 10 & 21 days
– Trypasamide 30 mg/kg iv every 5 days (total 12 inj)
• Can be repeated after 1 month
– Suramine 10 mg/kg iv every 5 days (total 12 inj)
• May be repeated after 1 month

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 Prevention
• Systematic surveillance
• Avoidance of stream & waterhole during warm,
dry season
• Eliminate flies at water crossing
• Restriction of travel in fly-interested region to
nighttime
• Use of headnets, legging,gloves
• Application of repellent
• Control of the tsetse flies
• High exposure : prophylaxis inj pentadimine
every 4-6 months
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Trypanosoma brucei
rhodesiense

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 Disease
• Rhodesian trypanosomiasis
• East African sleeping sickness

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Figure 2. Life cycle of Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense
 Epidemiology
• The incidence is lower and epidemics are
less frequent than in the Gambian
disease.
• Endemic among the cattle-raising tribes of
East Africa
• Tends to spread to new territory
• It is present in Zimbabwe, Zambia, Malawi,
Mozambique, Tanzania, and eastern
Uganda.
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 PATHOGENICITY
• More rapid & fatal course than Gambian disease
• Often terminating within a year
• Pathologic changes in acute disease ≈ Gambian
sleeping sickness
• Febrile paroxysms more frequent & severe
• Glandular enlargement <<
• Edema, myocarditis, weakness, & emaciation more
prominent
• Chronic lesions in CNS <<, since death intervenes
before marked cerebrospinal changes occur.
• Mental disturbances, tics, choreic movements,
convulsions, or the typical sleeping sickness syndrome
• Untreated cases  fatal
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 DIAGNOSIS
• Similar procedures as T. b. gambiense
– except that trypanosomes are more frequently
found in the blood
– more readily demonstrated by inoculation into
rats or mice

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 TREATMENT
• Requires earlier and more intensive
treatment
• Drug of choice in the early stages :
suramin

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 PREVENTION
• Involves medical, veterinary, entomologic, agricultural,
and social problems arising
• Redistribution of populations and the control of vectors
• Constant supervision to detect new cases, to keep track
of the old, to regulate agriculture
• Removal of inhabitants from fly-infested areas to open
country in close settlements
– By discriminative clearing of bush in essential fly habitats and in
the outer fringes of forests
– By spraying insecticides from airplanes
• Chemoprophylaxis, repellents, nets, screens

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Trypanosoma cruzi

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 DISEASES
• American trypanosomiasis
• Chagas’ disease.

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 MORPHOLOGY
• Long, thin form
– Length : 20 µ in
• Short, stumpy forms
– Length : 15 µ
• With pointed posterior ends
• In stained blood smears
– U or S shape
– A free flagellum : 1/3 of the body length
– A deeply staining central nucleus
– A large terminal kinetoplast
• In the tissues
– Round, intracellular amastigotes
– In small groups of cystlike collections

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 45
Figure 3. Life cycle of Trypanosoma cruzi
 EPIDEMIOLOGY
• Prevalent throughout South & Central
America
• Estimated 15 to 20 million persons
infected
• In endemic areas : Serologic surveys 15-
50% population is infected
• Prevalence is highest in the rural districts
and among the poorer classes living
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 PATHOLOGY &
SYMPTOMATOLOGY
• Infective trypanosomes  penetrate cells
of the mammalian host round up &
transform into amastigote forms 
repeated cycles of division  fill up the
cytoplasm of the cell  transform into
flagellate trypanosomes  infected cell
ruptures  liberating the actively motile
trypanosomal forms  invade new cells to
continue multiplication and some find their
way to the bloodstream
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 PATHOLOGY &
SYMPTOMATOLOGY
• Local lesion : chagoma
• Early stages
– Intracellular parasites are readily found in affected tissues,
sometimes in large cystlike collections, as well as free
trypanosomes in the blood.
– Glial cells of CNS and meninges can also become infected.
• Chronic stage
– Intracellular parasites diminish in numbers and trypanosomes
can no longer be found in the peripheral blood
– A great reduction in numbers of autonomic ganglion cells in the
muscle layers of hollow viscera and of the heart

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 PATHOLOGY &
SYMPTOMATOLOGY
• Clinical features
– Incubation period
• Fever, generalized lymphadenopathy
– Romafla's sign
– Hepatosplenomegaly
– Nondescript erythematous rash
– Acute disease usually subsides spontaneously
– Can be involve the heart or central nervous system
– Can be fatal.

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 DIAGNOSIS
• Endemic regions
– general, cardiac, or GI symptoms
• Direct examination of fresh anticoagulated blood or the centrifuged
buffy coat layer or in stained thick blood smears
– first month or two  T. cruzi be found
• Culturing the blood or suspected tissue specimen in N.N.N
• Xenodiagnosis
• Serologic tests
– Complement fixation
– Direct agglutination
– Indirect hemagglutination
– Immunofluorescence
– Immunoblots
– ELISA

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 TREATMENT
• Nitrofuran derivative
– Nifurtimox
• Benznidazole

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 PREVENTION

• destruction of the triatomid vectors

• protection of humans from their bites
• destruction of reduviid bugs in houses by
insecticides
• education, inspection of houses, and
insecticides

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LEISHMANIA

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 Classification
• Phylum : Protozoa
• Class : Mastigophora
• Order : Protomonadida
• Family : Trypanosomatidae
• Genus : Leishmania
• Species :
– Leishmania donovani
– Leishmania brasiliensis
– Leishmania tropica
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 MORPHOLOGY
• Small, oval, intracellular organism, 2 to 5 µ by 1 to 3 µ
• Amastigotes
– Found within phagocytic vacuoles of macrophages and other
mononuclear phagocytes.
– Nucleus & a rod-shaped kinetoplast
• Nearly 15% of the total cell DNA is packed into the
kinetoplast (kDNA)
• Promastigote
– In cultures or in the invertebrate host
– A long, delicate, anterior flagellum, varies from a pyriform to a
longer, slender spindle shape
– Size 14-20µ by 1.5-4.0 µ
– Reproduction : longitudinal binary division
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 56
Figure 4. Leishmania life cycle
 Leishmania donovani,
L. infantum and L. chagasi

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 DISEASES
• Kala-azar
• Black disease
• Visceral leishmaniasis
• Dumdum fever

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 MORPHOLOGY

• L. donovani
– In mammalian tissues
• a small, intracellular, nonflagellated oval body of uniform,
size-4.2 x 2.8 µ
– In the gut of infected sand flies or in cultures
• promastigote form
• L. infantum
– Causing kalazar in southern Europe & North Africa.
• L. chagasi
– Virtually indistinguishable from L. infantum
– Probably introduced to the western hemisphere by
Old World explorers or their dogs.

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 LIFE CYCLE
• Insect vectors
• Sand flies, Phlebotomus or Lutzomyia.
• In addition to humans, the dog is the most
important host.

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 61
Figure 5. Life cycle of Leishmania donovani
 EPIDEMIOLOGY
• Epidemiologic patterns
– the classic kalaazar of India
• adults; does not occur in dogs, and has no nonhuman
reservoir host
– the Mediterranean or infantile kala-azar
• sporadic in children : Mediterranean countries, China, Middle
Asia, Central & South America,
• occurs frequently in dogs & has wild reservoir hosts in jackals
and possibly foxes in Middle Asia and wild dogs in South
America
– kala-azar of Sudan, Kenya, Ethiopia
• adults; has rats, ground squirrels and gerbils as reservoirs.
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 PATHOLOGY &
SYMPTOMATOLOGY
• A primary lesion at the site of infection : rarely
• Africa : leishmaniomas
• Phagocytosed parasites
– in small numbers in the blood, but numerous in the
reticuloendothelial cells
• Incubation period 1 to 3 months, but it may be as short
as 2 weeks
• The onset is usually insidious and difficult to date
– Fever, sweating, weakness, weight loss, cough and abdominal
discomfort, enlarging spleen and liver
• In light-skinned patients hyperpigmentation of the skin
may be noted; the term kala-azar is Hindi for "black
sickness."

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 DIAGNOSIS
• Suspected
– in a patient who has a persistent, irregular, or
remittent fever, often with a double daily peak,
leucopenia and splenomegaly.
• Finding the paracite in stained smears
• Culture of bone marrow, splenic, hepatic,
or lymphnode aspirates.

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 TREATMENT
• Good nursing care
• Diet
• Appropriate antibiotics for secondary
bacterial infection
• Blood transfusion
• Th/ Pentavalent antimony

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 PREVENTION

• Treatment of infected person

• Elimination of disease dogs
• Sand flies may be controlled
– destruction of their breeding grounds near
human habitation
– use of insecticides
• Compactly built houses with fine mesh
screening
• Repellents
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 Leishmania tropica
L. major, and L. aethiopica

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 DISEASE
• Oriental sore
• Aleppo or Baghdad boil
• Old world cutaneous leishmaniasis
• recidivans or chronic relapsing cutaneous
leishmaniasis

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 MORPHOLOGY
• Amastigote & promastigote
– indistinguishable from L. donovani
• In smears from the cutaneous lesions : amastigotes
– intracellularly in mononuclear phagocytic cells
– extracellularly when released by the rupture of these cells
• The clinical forms of cutaneous lesion produced by anyone of the 3
species of parasite can be identical.
• L. tropica
– produce a dry lesion with late ulceration & the possibility of late
recurrence (recidivans form)
• L. major & L. aethiopica
– ulcerate early & have more exudation (the moist form)
• L. aethiopica rarely produce diffuse cutaneous leishmaniasis

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 LIFE CYCLE & EPIDEMIOLOGY
• L. major
– wide distribution in rural areas of southcentral
Russia, Afghanistan, Iran, the Middle East
• L. tropica
– same areast as L. major + Turkey & Greece restricted
more to urban centers
• L. aethiopica
– highlands of Ethiopia and Kenya.
• Vector : Phlebotomus
– P. papatasii
– P. sergenti
– P. longipes
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Figure 6. Leishmania tropica life cycle
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 PATHOLOGY AND
SYMPTOMATOLOGY
• Limited to cutaneous tissues & occasionally to mucous membranes
• Lesion
– Tiny reddish & often itchy papule that gradually enlarges
– A small serous discharge precedes ulceration of the skin
– Lesion enlarge, edges of ulcer raised & firm, dusky red surrounding skin
– Moist-type lesions remain open, with a sero-purulent. Exudate
– Dry-type lesions develop a crusted scab
• The parasites are found intracellularly in macrophages & histiocytes
• Incubation period 1 or 2 weeks to several months
• Single, multiple, metastatic lesions
• Secondary bacterial infection
• Generally systemic signs & symptoms are absent
• lesions not painful. no regional adenopathy
• Uncomplicated sores heal in 2 to 10 months

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 DIAGNOSIS
• Clinical feature
• Smears of biopsied tissues or scrapings of
the lesion edges
• Culture preferable for diagnosis
• Delayed intradermal reaction : positive
within several months after appearance of
the lesion and remains positive for years

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 TREATMENT
• Healing without chemotherapy can occur
• Th/ pentavalent antimony
– Sodium stibogluconate 15-20 mg/kg/day IM/IV
(15-20)
• a second or even a third course of treatment can
be given over 6 to 8 weeks if healing is not
progressive
– Ketoconazole 400 to 600 mg/day orally for
adults

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Leishmania mexicana and
Leishmania braziliensis
complexes

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 DISEASES
• American leishmaniasis
• Mucocutaneous leishmaniasis
• Espundia
• uta and chiclero ulcer.

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 LIFE CYCLE AND
EPIDEMIOLOGY
• Vectors :sand flies of the genus Lutzomyia
• Reservoir hosts are forest rodents and marsupials
• Occasionally, the domestic dog can be a reservoir
• L. mexicana & L. braziliensis complexes are distributed
from southern Texas, through Mexico, Central & South
America to northern Argentina.
• L. mexicana mexicana : predominant in Mexico is
• L. braziliensis braziliensis : the southern part of Mexico &
along the Atlantic side of Central America
• L. braziliensis panamensis : in Central & northern South
America
• L. mexicana amazonensis : northern & central South
America
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 78
Figure 7. Leishmania braziliensis life cycle
 PATHOLOGY AND
SYMPTOMATOLOGY
• Clinical appearance & histopathology ≈ that of oriental sore
• Except : some of the American forms may produce later mucous
membrane involvement
• The organisms can metastasize  development of nearby satelite
lesions or subcutaneous nodules in a linear drainage pattern
• Regional adenopathy is variable.
• Mucosal lesion: nasal obstruction, bleedingpainful, great deformity
• The form of disease with mucosal features is called espundia.
• DCL, or diffuse type : unusual form of leishmaniasis
• PCL
• The nonulcerating chronic skin lesions ≈ those of lepromatous
leprosy

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 DIAGNOSIS

• Clinical appearance
• Aspirated or scraped from the edge of
lesions
– smear
– Culture.
• Biopsied tissue is best.
• A positive intradermal Montenegro test
using antigen
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 TREATMENT
• Pentavalent antimony (Sb+5) 20 mg/kg
daily (15-20 days)
• Ketoconazole 400-600 mg/day
• Amphotericin B 0.25-1 mg/kg IV, daily or
every other day, for a total dosage of 1.5
to 2.5 g for adults.

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Toxoplasma gondii

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 Classification
• Phylum : Protozoa
• Class : Sporozoa
• Order : Coccidia
• Genus : Toxoplasma
• Species : Toxoplasma gondii

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 History
• 1908 : first found in the African rodent
Ctenodactylus gondii
• 1923 : Janku described toxoplasmic
chorioretinitis
• 1939 : Wolf, et al. isolated the parasite,
estabilished as the cause of congenital
neonatal disease

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 Morphology
• Obligate intracellular parasite
• Pyriform
• Size : 3 x 6 µ
• Cell membrane, nucleus, organelles

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 Morphology
• Oocyst
– Diameter : 10-13µ
– 2 layers
– Contain undefferentiated material
– Contents  2 sporocysts
– Sporocysts  4 sporozoites

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Figure 9. Life cycle of Toxoplasma gondii 87
 Epidemiology
• Cosmopolitan
• 20-75% chronic but asymptomatic
• Mode of transmission
– Via ingestion of partially cooked or raw meat
– Transplacental
– Oocysts ingested directly
– By aerosol dispersion
– Drinking water contaminated by oocyts
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 Pathology & Symptomatology
• Congenital Toxoplasmosis
– 1-5 per1000 pregnancies
– Severe, even fatal
– Varying degree of severity
• 5-15% die
• 8-10% severe brain & eye damage
• 10-13% moderate to severe visual handicaps
• 58-72% asympromatic

89
Pathology & Symptomatology
– Typical syndrome
• Intracerebral calcification
• Chorioretinitis
• Hydrocephaly
• Microcephaly
• Psychomotor disturbance
• Convulsion

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 Pathology & Symptomatology
• Acquired or Reactivated Toxoplasmosis
– 2 main clinical types
• Mild lymphatic form
– More common
– Lymphadenopathy,malaise, muscle pain, fever
• Acute, fulminating, disseminated infection
– Skin rash, high fever, chills, prostrations,
meningoencephalitis, hepatitis, pneuminitis

91
 Pathology & Symptomatology
• Opportunitic infection
– Organ transplantation
– AIDS
– Certain neoplastic disease

92
 Diagnosis
• Serologic test
– ELISA
– Indirect immunofluorescent
– Complement fixation test
• Inoculation into mice or cell culture
• Polymerase chain reaction (PCR)

93
 Treatment
• Symptomatic infection
– Pyrimethamine
• Adult : 25-50 mg/day orally for 3-4 weeks
– Trisulfapyrimidine
• Adult : 2-6 g/day orally for 3-4 weeks

94
 Prevention
• Washing hands with soap and water after
handling meat
• Cooking of all meat
• Careful attention to cat feces

95