Advanced Parasitology Lecture1, Introduction

PRINCIPLES OF PARASITOLOGY
(Biol.3081)
3 Credits
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INTRODUCTION
Parasitology is the study of parasites and their interactions with their hosts
 The science of parasitology has a long history and has its root in
• Zoology, with its emphasis with identification and classification of

parasites and the elucidation of the parasite life cycles, and
• Tropical and Veterinary Medicine with their concern for diseases caused
by parasites
 However, the subject is now so intertwined with microbiology,immunology,cell
biology,molecular biology and other aspects of biology and medcine
 Parasitology is the science that deals with one of several different kinds of
symbiotic relationships.
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Taxonomy and nomenclature of parasites
A. Taxonomy
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CONCEPTS OF PARASITISM
 Is parasitism a form of animal association? If so how does our concept of
parasitism differ from other associations, say prey/predator interactions?
 Animal associations:-The majority of animals live independently in their
natural habitats, seeking their own food materials and utilizing free water
and oxygen for their metabolic processes.
• Between some animals, however, a variety of patterns of association have

developed, and these may be broadly divided into two groups:
• Homogenetic associations those between individuals of the same

genotype; and
• Heterogenetic associations - those between individuals of
different genotype
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Cont…
 In Homogenetic associations:-
 Individuals of the same species may form loosely united communities,

such as herds of cattle or flocks of sheep,
 While others, such as some species of ants or bees, may form
elaborately organized communities in which individual members often
exhibit considerable division of labor or specialization
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SYMBIOSIS
• Means literally living together which covered a range of intimate
interactions between organisms
• A functional separation can be made in terms of trophic relationships
and then, if and how energy is transferred between symbiotic
organisms
• The most common ones being phoresy, commensalism, mutualism,
and parasitism.
• So, most modern literature has now returned to using symbiosis as an
umbrella term for organisms that live together.
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1. PHORESIS : No trophic interaction
 No trophic interaction between the organisms in the symbiotic
relationship, then the relationship is called Phoresy
 That means, one organism provides shelter, support or transport for
another organism of a different species
• The classical examples: Butterfly and pollen.
2.COMMENSALISM:The term literally means 'eating at the same table‘.

Involves one way benefit, but as in the case of mutualism no harm is
exerted in either direction
• There is a trophic relationship and a transfer of energy b/n symbiont
• The benefit gained is unidirectional, one partner benefits and the other is
neither harmed nor helped
• Commensalism usually involves a feeding relationship and generally does
not involve metabolic dependence 7
Cont….
• In many cases, although this type of association is beneficial to one or
both organisms, it is not usually obligatory for their existence.
• Commensalism may thus be considered a type of loose association in
which two animals of different species live together without either being
metabolically dependent on the other, although one or both organisms
may receive some benefit from the association.
Examples: Clown Fish and sea-anemone: The sea anemone provides

protection against predators; the clown fish is highly evolved to survive
the cnidarian nematocysts.
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3.MUTUALISM: two way benefit, no harm
 When there is direct transfer of nergy b/n the partners, the interacion may
be either Mutualistic or Exploitative
• In a mutualistic relationship, both symbionts not only obtain benefit, but
neither can survive without the other
• Highly interdependent association, to the extent that the two associates
cannot survive without one another
• Lichens are a classic example of an obligatory association between a
fungus and an alga. The fungus provides protection and moisture for the
alga and the alga in turn provides nutrients for the fungus.
• The r/shp b/n ruminants and the microorganisms in their stomach is also
mutualistic
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4.PARASITISM:one way benefit
 In most exploitative interactions benefit is in one direction and some
form of disadvantage, or harm, is the outcome for the other partner
• Several major catecories of this kind of exploitation can be recognized
based on the number of hosts attcked by the symbiont and the subsequent
fate of the organism assaulted:micropredator,predator,parasitoid and
parasite
 If more than one organism is attacked, but typically not killed, then the
aggressor is called a micropredator
• Example of micropredators: Hematophagous organisms, such as
mosquitoes, and some leeches and biting flies
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Cont….
 If more than one organism is attacked and always killed, then the
aggressor is considered a predator
 If only one host is attacked and always killed, then the aggressor is
usually referred to as a parasitoid, most of which are hymenopterans
and dipterans
• Examples of parasitoids, adult female wasp may deposit her eggs(s) on,
or into, an insect. On hatching, the larval parasitoid will consume the
host, killing it in the process
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Cont....
 If only one host is attacked, but is not killed, the aggressor is a parasite
• Many parasites have free-living stages in their life cycles and only during
the periods when they make contact with their hosts can they actually be
considered to lead a parasitic existance
• Of all the types of animal associations, perhaps the tetm parasitism has
been the most difficult to descirbe. Because the term has a relative meaning
• Parasitism is an intimate relationship between two organisms in which
one (the parasite) lives on, off or at the expense of the other (host)
• This implies that one of the partner benefits, the other is harmed
• One problem with this simple definition is that harm is a very difficult thing
to quantify
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Cont...
 The relativity of parasitism depends on the following factors:
a) the intimacy of the association,
b) its pathogenic effect,
c) its metabolic or physiological dependence,
d) whether or not the host 'recognizes' the parasite as 'foreign',
e) the ability of the parasite to 'recognize' the host site as being a

suitable ecological niche.
 These factors are not, of course, independent, and complex interactions
between them may occur in any particular host-parasite situation
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Cont...
A more recent definition or perhaps description of parasitism
i. Ecological relationship between two different organisms, one
designated the parasite, the other the host.
ii. The parasite is physiologically or metabolically dependent upon its

host.
iii. Heavily infected hosts will be killed by their parasites.
iv. The reproductive potential of the parasite exceeds that of their hosts.
v. There is an over dispersed frequency distribution of parasites within the

host population. That is, the parasite population is not evenly
distributed amongst the host population nor is it randomly distributed
but clumped, so some hosts have a lot of parasites, most have very few
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PARASITE
• Parasites exhibit combinations of biochemical, physiological and
nutritional adaptations unique in the animal world and also
display a range of mechanisms for evading the immune
responses of the host unknown to other pathogen
• Their ecology is also far more complex than that of free-living
organisms
• In biology, a parasite is an animal or plant living in or on another
(the host) and drawing nourishment from it. That means, a
parasite is an organism that lives a significant period of its life in
or on another organism (the host), from which it obtains
nourishment and shelter
• This definition could include viruses, bacteria and fungi as well
as protozoa and helminths, but historically the first group has
been studied in microbiology, the second in parasitology
• In the broadest sense, all viruses, and many bacteria and fungi
are parasitic, but traditionally most parasitologits focus on
eukaryotic animal parasites
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Metaboloc dependance
• A parasite is not only in continous, intimate association
with another organism, the host, but is also
metabolically dependant, directely or indirectly, on it
to some degree.
• The relative nature of this association can be seen on
the degree of metabolic dependance of a parasite on
its host
• A free living organism shows zero dependance, wheras
a blood-dwelling protozoan (e.g. Plasmodium) is 100%
dependent. In between these two exteremes lies a
range of organisms which satisfy their metabolic
requirements to a varying extent at the expense of the
host 16
Free-living Totally parasitic
0% 100%
What we mean by metabolic dependance?

Parasites are dependent on their hosts for one or more of the
following:
a) Developmental stimuli
b) Nutritional materials
c) Digestive systems
d) Control of maturation and (more rarely) mitosis
Parasites have also different
o Morphological
o Physiological
o Bichemical and
o Immunological adaptation mechanisms 17
A cartoon-like representation of an ideal parasite
1. Recognition of Habitat: Recognizes a
host site suitable for establishment;
2. Maintenance: Maintains its position
there;
3. Physico-chemical: Is adapated to the
physioco-chemical conditions of the
host
4. Nutritional: Utilizes host nutrient in a
manner compataible with host
survival;
5. Molecular mimicry: Presents a surface
with a molecular configuration such
that host immune response is absent
or minimized;
6. Parasite and host cycles linked: has a
life cycle synchronised with that of the
host
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Kinds of Parasites
 Parasites can be classified according to their life cycles, position in or on
the hosts, size, or other features
 Ectoparasite:- lives on surface;typically confined to the exterior of the
host’s body
– They live on the outside of their hosts, usually attached to the skin,
feathers, hair, gills, e.t.c
– Most parasitic arthropods (e.g., fleas, lice, ticks) and most
monogeneans are ectoparasitic
 Endoparasite:- live inside host in the gut, body cavity, lungs or other
tissues
– Include those parasites that are confined within the host’s body
– They include protozoans, digeneans, cestodes, nematodes, and
acanthocephalans
– Many bacteria and all viruses are also endoparasitic
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Cont...
 Mesoparasite:- Certain parasites fall in to both these groupings
– penetrates external openings - buccal cavity, cloaca, external ear
– Example:- The itch mite (Sarcoptes scabei), burrows in tunnels in the skin
and could satisfy the cretieria of either an ectoparasite or an endoparasite
 Macroparasites:-Are large and can be viewed without the aid of a
microscope;can be endoparasitic, such as digeneans, cestodes, nematodes, and
acanthocepalans, or ectoparasitic, such as arthropods and monogeneans
 Microparasites:-Are mostly microscopic and can be ectoparasitic or
endoparasitic
– They may also be intracellular, or extracellular, or both
– Eukaryotic microparasites are primarily protozoans
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Cont...
 Obligate parasite:- are organisms obliged to live a parasitic existence
– Are incapable of surviving outside the host environment (naturally

occuring environment)
 Facultative parasites:-Organisms which can live either a parasitic or
non-parasitic existance
 Hyperparasites (Hyperparasitism):-Parasites can have parasites too
– These parasites of parasites are called hyperparasites
– Hyperparasites are usually bacteria or viruses, but some protozoans,

cestodes and crustaceans have been found parasitizing other parasites
 Incidental Parasite – can utilize a different host
 Aberrant Parasite– In an usual host or location 21

Kinds of Hosts and Life Cycles
Host: An organism that harbors and provides sustenance for another
organism (the parasite).
Definitive (Final) host:- harbours adult stage where parasite reaches sexual
maturity, i.e., the organism in, or on, which a parasite reaches sexual maturity
– Some parasite require one host to complete their life cycles.
– These cycles are said to be direct life cycle
– All monogeneans, and some nematodes and arthropods, have direct life
cycle
Intermediate host:-
– Harbours larval stage (s)
– is a temporary environment for the parasite, but is nonetheless
necessary for the parasite to complete its life cycle
– They often can undergo asexual reproduction in this type of host.
– usually undergoes morphological or physiological change in it, but do
not reach sexual maturity
– Life cycles in which more than one host is required are indirect life
cycles
22
Cont..
 Biological Vectors:- host that plays an active role in transmission,
– can be a definitive or an intermediate host, depending on whether the

sexual phase of the parasite’s life cycle occurs in it or not
– Are micropredators that transmit infections from one host to another
 Paratenic (transport) host:- optional transport host - no detectable

morphological change in parasite
– Hosts in which there is no development and that are not always
obligatory for the completion of a parasite’s life cycle
– Such hosts are most frqently used to bridge an ecological, or trophic,
gap
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Cont…
 Reservoir hosts:-Animals that harbor an infection that can be transmitted to
humans are referred to as reservoir hosts
– Serving as a source of infection for others
 Infection: – Parasites (endoparasites) inside a host
 Infestation: – Parasites (ectoparasites) on a host
 Infection vs Disease (-iasis, -osis, -os) : clinical or subclininical
• Parasites may occur without causing disease
 The essence of parasitism rests with the nature of host-parasite relationships
 Parasitism is an ecological concept i.e is essentially a branch of ecology in

which the habitat and environment of an organism (the parasite) is provided
by another organism (the host)
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Ecology (Niches, Habitats and Environment) and Host-Parasite
Relationship
• The phenomenon of parasitism can be considered as an ecological

relationship between two populations of different species
• Ecologically, the host parasite relationship is a double-edged sword
• Because dealing with parasites and their hosts from an ecological

perpective, one must simultaneously consider the ecology of the host(s)
in a parasite’s life cycle, as well as the host as a habitat for the parasite
• Many of the biotic and abiotic vagaries affecting the ecology of the host
will also affect the parasite
• But the parasite also must deal with a host that is alive, and capable of
responding physiologically and immunologically to the parasite
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Cont…
• Niches:-it refers to the space in the biotic environment in which life is
possible
– Fundamental niche is the unique combination of environmental
factors, biotic and abiotic, which are capable of supporting life
• Habitats:- The environmental components of the niche
– Examples:- alimentary canels or gills of fishes. It is possible that two

different species of parasites to occupy the same habitat (e.g.
Intestine) while occupying different niches, becuse one utlises
glucose as a nutritional substances, whereas the other utlises
fructose; they thus occupy different (nutritional) niches
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Cont…
The Fovered Habitats in Vertebrates are:-
– The alimentary canal and associated glands,blood stream, respiratory
system and coelom
The less common ones in vertebrates:

– The nervous systems and its derivations,excretory system, and
reproductive system
• In the invertabrates, possible habitats are fewer, but most tissues have
been invaded, especially by vector stages of protozoa or larval stages of
helminths
• Environmental conditions affecting the development of the parasite
• The physioco-chemical conditions of a habitat

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Life cycle
Monoxenous parasites:
– Requiring only a single host to complete the life cycle.
– Have a direct life cycle (E.g. Ascaris lumbricoides)
Heteroxenous parasites:
– Those which require two or more hosts to complete their life cycle
(E.g. Plasmodium species)
– Have indirect life cycle (require an intermediate host)
Heterogenetic parasites:
– One with alteration of generations e.g., Coccidial parasites and
Strongyloides
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Ecology (Niches, Habitats and Environment) and Host-
Parasite Relationship
Environmental conditions affecting the development of
the parasite
• The physioco-chemical conditions of a habitat
– pH,
– pCO2
– Oxygen tention
– Oxidation-reduction potential
– Temperature
– Viscosity
– Osmotic pressure
• The nature, quantity and availability of food materials
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How parasite transmit and cause disease in Man
Transmission of parasites requires:-
1. a source (reservoir), human or animal
2. a mode, for example ingestion, penetration, an insect vector
Parasites cause disease in man by:

1. Mechanical effects, for example hydatid cyst
2. Invasion and destruction of host cells, as in malaria
3. Allergic or inflammatory immune reaction by the host to the
parasite, through a cellular or a chemical reaction, or both, for
example trichiniasis, trypanosomiasis
4. Competition for specific nutrients, for example D. latum for
vitamin B12
5. Or their may be no obvious disease, as in T. saginata in man30
Estimates of current human infections (and distributions) caused by
the major parasitic organisms
Disease Numbers in Distribution (Primary)
millions
Hookworm 1298 Cosmopolitan
Ascariasis 1472 Cosmopolitan
Trichuriasis 1050 Cosmopolitan
Filariasis 100 Asia; SW Pacific Islands
Onchocerciasis 18 C. & S. America; S.S. Africa
Paragonimiasis 21 Asia; S. Africa
Schistosomiasis 200 Asia; Africa
Strongyloidiasis 70 Cosmopolitan
Malaria 300 Asia; S.S.Afri; C. & S. America
Leishmaniasis 80 Asia; S.S.Afri; C. & S. America
Chagas’ disease 18 C. & S. America
African trypanosomiasis 20 S.S. Africa
Amoebiasis >500 Cosmopolitan
Giardiasis 200 Cosmopolitan 31
Amoebiasis
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Gardia lamblia Infection
in Jejunal Ethithelium
Other Parasitic
Flagellates
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34
MALARIA
MALARIA
35
MALARIA
36
MALARIA 37
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LEISHMANIASIS
Leishmaniasis
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40
Morphological Differentiation of
Protozoans
ROUND WORMS
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Schistosomiasis
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WHIPWORMS
Filarial worms
44
Onchocerciasis
45
Guinea Worm
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ARTHROPODS
47
Parasitic diseases
Factors influencing the pathogenic potential of a parasite
• The migratory pathway in a host
• The predilection where a parasite develops
• Feeding habits
• Propensity to stimulate hyperactive immunological
responses
– Fibrosis,
– granulomas,
– autoimmune and allergic reactions,
– splenomegaly etc.
• The potential of a parasite to transmit other infectious
agents (eg. ahropods)
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Parasite Immune Response
• The nature of the immune response to parasites is
variable and may be:
– Non-specific and non-effective immune stimulation without the
formation of protective antibodies, for example
trypanosomiasis, visceral leishmaniasis, amoebiasis
– Partial but non-sterilizing immunity which modifies the disease
to a controlled level (premunition), for example, malaria in
endemic countries
– Immunity protecting against new infection but not killing
existing parasites (concomitant immunity), for example in
schistosomiasis
49
Parasite Immune Response
• The nature of the immune response to parasites
is variable and may be:
– Sterilizing immunity preventing new infection, as in

cutaneous leishmaniasis
– The immune response by the host is usually specific to

the species of parasite concerned and may be further
specific to a given strain of the parasite or to a
particular stage of the life cycle (for example ova in
schistosomiasis, sporozoites in malaria).
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How Parasites Escape the Host Immune System?
Parasites are capable of partial or complete evasion of
the immune attack on them by various means:
• Anatomical seclusion
– Intracellular, for example malaria hypnozoites
– Intraluminal in gut, for example tape and round worm
adults.
• Self-modification of antigenicity, as in malaria, trypanoso
miasis, amoebiasis, schistosome adults
• Induction of modified host response, for example
immunosuppression by malaria, modified white blood
cell function by leishmaniasis
51
Diagnosis
Diagnosis in parasitic disease depends on:
• A history of exposure and the clinical pattern of illness
in the patient
• Identification of the parasite itself in excreta (stool,
urine), blood, or specific tissues. This is the most
important method of diagnosis
• Indirect evidence of the parasite by testing the
patient's blood for antibodies, for example:
– precipitation
– agglutination
– indirect haemagglutination (IRA)
– complement fixation (CFT)
– immunoelectrophoresis (IEP)
– immunofluorescence (IF)
– enzyme-linked immunosorbent assay (ELISA) 52
Diagnosis
• Although such tests may be nonspecific because of the
lack of precise knowledge of the antigens, causing
'cross-reaction' of species.
• Detection of circulating parasite antigens in the blood of
the patient. At present this is a difficult technique
because such antigens are in low concentration but
newer tests using monoclonal antibodies will make this
method more accurate
• Detection of circulating complexes of antigen and
antibody in the blood of the patient
• The use of skin tests for hypersensitivity to parasite
antigen, for example Casoni test for hydatidosis
53
Prevention and control
Prevention and control of parasitic disease depends on:
• Reduction of the human source of infection by drug
treatment, e.g. malaria, onchocerciasis
• Personal prophylaxis in avoidance of transmission, for
example malaria
• Community control of water, food and sanitation, for
example schistosomiasis, dracontiasis
• Destruction or control of animal hosts and insect
vectors, for example mosquitoes in malaria and meat
inspection in trichiniasis
• Erection of biological barriers to transmission, for
example fish species which destroy mosquito larvae54
CLASSIFICATION OF PARASITES
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CLASSIFICATION OF PARASITES
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57
QUIZ1
INTESTINAL & UROGENITAL
PROTOZOA
LECTURE 2
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Table 1.2 Classification of the protozoa
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PROTOZOOLOGY
Introduction
• The Protozoa contains unicellular organisms, which
belong to the Kingdom Protista.
• Obtain their energy by the intake of organic material
(majority do not have photosynthetic ability)
• Protozoa are more primitive than animals, and all the
different structures are contained in a single cell.
• Protozoa, like most organisms, are eukaryotic, in that
their genetic information is stored in chromosomes
contained in a nuclear envelope.
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STRUCTURE AND FUNCTION OF PROTOZOA
• Protozoa, like other eukaryotic cells, have a

nucleus, an endoplasmic reticulum,
mitochondria and a Golgi body and lysosomes.
• In addition, because they lead an independent
existence they possess a variety of other sub-
cellular structures or organelles with distinct
organisational features and functions.
63
Locomotion
• In the genus Trypanosoma locomotion is facilitated
by a single flagellum, and in some other protozoa by
several flagella.
• A flagellum is a contractile fibre, arising from a
structure called a basal body, and
• In some species the flagellum is attached to the body
of the protozoan along its length, so that when the
flagellum beats, the cell membrane (pellicle) is pulled
up to form an undulating membrane.
• Sometimes, also, it projects beyond the protozoan
body as a free flagellum. During movement the
shape of these organisms is maintained by
microtubules in the pellicle.
64
Locomotion continued
• Other protozoa, such as Balantidium move by means
of cilia which are fine, short hairs, each arising from a
basal body; these cover much of the body surface and
beat in unison to effect movement.
• In such species a mouth or cytostome is present and
the ciliary movement is also used to waft food towards
this opening.
• A third means of locomotion, used by protozoa such as
Entamoeba are pseudopodia, which are prolongations
of cytoplasm. Movement occurs as the rest of the
cytoplasm flows into this prolongation.
65
Fig. 1.47 The morphology of
the intestinal protozoan
Balantidium
Fig. 1.46 Trypanosoma

brucei showing the flagellum
and undulating membrane.
Fig. 1.48 Entamoeba histolytica has an

amoeboid trophozoite stage and a non-motile
cystic stage with four nuclei. 66
Locomotion continued
• The pseudopodium also possesses a phagocytic
capacity and can function as a cup, which
closes, enveloping particulate food material in a
vacuole.
• Some protozoa, such as the extracellular stages

of the Eimieria, have no obvious means of
locomotion, but are nevertheless capable of
gliding movements.
67
The nutrition of parasitic protozoa
• The nutrition of parasitic protozoa usually occurs by pinocytosis
or phagocytosis, depending on whether tiny droplets of fluid or
small objects of macromolecular dimension are taken into the
cell.
• In both cases, the process is the same, the cell membrane
gradually enveloping the droplet or object which has become
adherent to its outer surface.
• When this is complete, the particle is carried into the cell where
fusion with lysosomes effects digestion.
• Finally, undigested material is extruded from the cell.
• Some ciliated protozoa and also some stages of the organisms
causing malaria obtain food through a cytostome.
• At the base of the cytostome the food enters a vacuole for
digestion within the cell. Metabolic products are excreted by
diffusion through the cell membrane.
68
Reproduction and the infective stage of protozoa
• The infective stage of some protozoa is called a sporozoite,
while the term trophozoite is applied to that stage of the
protozoa in the host, which feeds and grows until division
commences.
• In most protozoa, reproduction is asexual and is accomplished
by binary fission or, in the case of Babesia within erythrocytes,
by budding.
• Another form of asexual reproduction, which occurs in the
subphylum Sporozoa is merogony (schizogony). In the latter
process, the trophozoite grows to a large size while the nucleus
divides repeatedly.
• This structure is called a meront (schizont) and, when mature,
each nucleus has acquired a portion of the cytoplasm so that the
schizont is filled with a large number of elongated separate
organisms called merozoites. The meront eventually ruptures,
liberating the individual merozoites.
69
Reproduction cont’d
• Protozoa that only divide asexually generally have a
short generation time, and since they cannot exchange
genetic material, rely on mutants to provide the
variants necessary for natural selection.
• However, most Sporozoa at certain stages in their life
cycle also have a sexual phase of reproduction, called
gametogony, which may be followed by a free-living
maturation phase, or sporogony.
• Some times, as in Eimeria, both asexual and sexual
phases occur in the same host while in others, such as
Plasmodium, the asexual phase occurs in the
vertebrate host and the sexual phase in the arthropod
vector.
70
Fig. 1.50 Life cycle of Eimeria.
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CLASSIFICATION
• Classification of the subkingdom Protozoa

(kingdom Protista) is extremely complex
• There are four phyla of protozoa of Medical and

Veterinary importance, the
Sarcomastigophora, Apicomplexa (Sporozoa),
Microspora and Ciliophora.
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Intestinal Protozoa
73
Protozoa with locomotion by Pseudopoda
and/or flagella
74
Members move by means of Pseudopods
which also used for feeding
Cytoplasm divided into
i) Endoplasm- containing food vacules, and
ii) Relatively clear ectoplasm
Reproduction is asexual by binary fission
Only few species of Sarcodina are pathogenic
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76
INTESTINAL AND UROGENITAL
PROTOZOA
• Intestinal and luminal protozoa significant to
human health include
– Entamoeba histolytica (Amebae)

– Balantidium coli (Ciliates)
– Giardia lamblia and Trichomonas vaginalis
(Flagellates)
– Cryptosporidium parvum and
– Isospora belli (Sporozoa)
77
Family ENDAMOEBIDAE
• Members of this family are parasitic in the
digestive tract of vertebrate and invertabrate
• Three genera contain parasites of animals and man
i) Entamoeba
ii) Iodamoeba
iii) Endolimax
• But only Entamoeba contains pathogenic species
of medical and veterinary significance
• Genera are differentiated on the basis of their
nuclear structure
78
AMEBIASIS (amebic dysentery, amebic hepatitis)
• Etiology
– E. histolytica is the major cause of amebic dysentery.
– Parasitic amoeba (Entamoeba histolytica) causes
amebic dysentery & ulcers (vegetative trophozoite
stage).
– Amebic dysentery is spread by fecal contamination
of food and water and is most common where
sanitation is poor.
79
AMEBIASIS (amebic dysentery, amebic hepatitis)
• Epidemiology
– 0.5 to 50% of the population world wide harbors E.

histolytica parasites with the higher rates of infection
being in underdeveloped countries.
– 1 to 3% of the population of the USA is infected.
– Infection is associated with poor hygiene.
– Humans are the principal host, although dogs, cats
and rodents may be infected.
80
Morphology
• Trophozoite:
– This form has an ameboid appearance and is usually
15-30 micrometers in diameter, although more
invasive strains tend to be larger
– The organism has a single nucleus with a distinctive
small central karyosome
– The fine granular endoplasm may contain ingested
erythrocytes
– The nuclear chromatin is evenly distributed along the
periphery of the nucleus
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Entamoeba histolytica
Trophozoite
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Trophozoite Trophozoite
Trophozoite 83
Trophozoites of Entamoeba histolytica
• The trophozoites are elongated (up to 60 µm in
length), as they tend to be in diarrheal stool.
• In non diarrheal stool, they are more rounded,
and measure 15-20 µm.
• The nuclei show a centrally placed karyosome
with a uniformly distributed peripheral chromatin
84
85
Cyst Cyst
86
Morphology
Cyst:
– Entameba histolytica cysts are spherical, with a
refractile wall;
– The cytoplasm contains dark staining chromatoidal
bodies and
– 1 to 4 nuclei with a central karyosome and evenly
distributed peripheral chromatin
– Each cyst has 4 nuclei
– The nuclei have characteristically centrally located
karyosome.
– The cyst contains a large chromatoid body.
– Entamoeba histolytica cysts measure 12-15 µm 87
LIFE CYCLE
• Infection occurs by ingestion of cysts on fecally
contaminated food or hands.
• The cyst is resistant to the gastric environment and
passes into small intestine where it decysts.
• The metacyst divides into four and then eight amoebae
which move to the large intestine.
• The majority of the organisms are passed out of the
body with the feces but, with larger bolus of infection,
some amebae attach to and invade the mucosal tissue
forming "flask-shaped" lesions (bomb craters).
• The organisms encyst for mitosis and are passed
through with feces
• There are no intermediate or reservoir hosts. 88
LIFE CYCLE
89
LIFE CYCLE
• Infection by Entamoeba histolytica occurs by ingestion
of mature cysts (1) in fecally contaminated food, water,
or hands.
• Excystation (2) occurs in the small intestine and
trophozoites (3) are released, which migrate to the large
intestine.
• The trophozoites multiply by binary fission and produce
cysts (4) , which are passed in the feces.
• Because of the protection conferred by their walls, the
cysts can survive days to weeks in the external
environment and are responsible for transmission.
90
LIFE CYCLE
• Trophozoites can also be passed in diarrheal stools, but
are rapidly destroyed once outside the body, and if
ingested would not survive exposure to the gastric
environment.
• In many cases, the trophozoites remain confined to the
intestinal lumen (A: non-invasive infection) of
individuals who are thus asymptomatic carriers and
cysts passers.
• In some patients the trophozoites invade the intestinal
mucosa (B: intestinal disease), or, through the
bloodstream, extraintestinal sites such as the liver,
brain, and lungs (C: extra-intestinal disease), with
resultant pathologic manifestations.
91
LIFE CYCLE
• It has been established that the invasive and
noninvasive forms represent separate species,
respectively E. histolytica and E. dispar, which
are morphologically indistinguishable.
• Transmission can also occur through fecal
exposure during sexual contact (in which case
not only cysts, but also trophozoites could prove
infective)
92
SYMPTOMS
• Acute:
– Frequent dysentery with necrotic mucosa and
abdominal pain.
• Chronic:
– Recurrent episodes of dysentery with blood and
mucus in the feces.
– There are intervening gastrointestinal disturbances
and constipation.
– Cysts are found in the stool.
– The organism may invade the liver, lung and brain
where it produces abscesses that result in liver
dysfunction, pneumonitis, and encephalitis.
93
PATHOLOGY
• Intestinal ulcers (craters/flasks) are due to
enzymatic degradation of tissue.
• The infection may result in
– appendicitis,
– perforation,
– stricture granuloma,
– pseudo-polyps,
– liver abscess;
– sometimes brain, lung and spleen abscesses can also
occur.
• Strictures and pseudo-polyps result from the host
inflammatory response. 94
HISTOPATHOLOGY
Histopathology of a typical
flask-shaped ulcer of Gross pathology of liver
intestinal amebiasis containing amebic
abscess
95
HISTOPATHOLOGY
Skin abscess
Gross pathology of amebic abscess

of liver. Tube of "chocolate" pus from
abscess.
96
IMMUNOLOGY
• There is an antibody response after invasive

infection (liver abscess or colitis) but it is of
questionable significance in immunity, as there
is recurrence of enteric episodes in these
patients.
97
DIAGNOSIS
• Symptoms, history and epidemiology are the keys to
diagnosis.
• In the laboratory, the infection is confirmed by finding
cysts in the stool.
• E. histolytica infection is distinguished from bacillary
dysentery by the lack of high fever and absence PMN
leukocytosis.
• Distinction must be made from other non-pathogenic
intestinal protozoa (e.g., Entamoeba coli, Entamoeba
hartmanni, Dientamoeba fragilis, Endolimax nana,
Iodamoeba buetschlii, etc.)
98
TREATMENT
• Iodoquinol is used to treat asymptomatic

infections and
• Metronidazole is used for symptomatic and

chronic amebiasis, including extra-intestinal
disease
99
Non-Pathogenic Intestinal Protozoa
1. Entamoeba coli: Trophozoite
• Trophozoite, stained in trichrome,
showing a characteristically large,
eccentric karyosome, and a
coarse, vacuolated cytoplasm.
• The trophozoites of E. coli
measure usually 20-25 µm, but Cyst
they can be elongated and reach
50 µm.
• Mature cysts typically have 8
nuclei, and measure usually 15 to
25 µm (range 10 to 35 µm).
100
1. Entamoeba coli:
• Entamoeba coli cyst and
trophozoite, haematoxylin stained
• Entamoeba coli trophozoite,
trichrome stained
• Entamoeba coli: Trophozoite,
stained in trichrome, showing a
characteristically large, eccentric
karyosome, and a coarse,
vacuolated cytoplasm.
101
2. Entamoeba hartmanni:
• Cyst, with one nucleus visible at this focal
plane; again rather similar to cysts of E.
histolytica, but differentiated by their smaller
size (5-10 µm compared to 10-20 µm)
• Trophozoites stained in trichrome : the
trophozoites of E. hartmanni are rather
similar to those of E. histolytica, with a small,
often centrally located karyosome, fine
peripheral chromatin, and finely granular
cytoplasm;
• The main difference is in their small size: 5-
12 µm compared to 10-60 µm for E.
histolytica. Note that the trophozoite has
ingested a yeast, not an erythrocyte.
• Ingestion of erythrocytes is pathognomonic
of E. histolytica
102
3. Endolimax nana: A
• Trophozoite stained in trichrome (A) and cysts
stained in iodine (B) and in trichrome (C).
• Note in the trophozoite the characteristically
large blot-like karyosome, and the lack of
peripheral chromatin. B
• The cysts are mature, they contain four nuclei
that are much smaller than the nuclei of the
trophozoites and do not have peripheral
chromatin.
• The trophozoites are usually 8-10 µm in size, C
while the cysts are usually 6-8 µm.
103
A
4. Iodamoeba bütschlii:
• Trophozoites stained in trichrome (A)
and in hematoxylin-eosin (B), and cyst
stained in trichrome (C).
• Note the large karyosomes in the B
trophozoites, and in (B) the karyosome
surrounded by refractile achromatic
granules.
• In the cyst (C), a large mass of glycogen
pushes the nucleus aside.
• The trophozoites are usually 12-15 µm in
size, and
• The cysts are usually 10-12 µm C
104
A
5. Dientamoeba fragilis :
• Trophozoites, trichrome stain.
• Dientamoeba fragilis is not an
ameba, but a flagellate!
• It must be however morphologically
differentiated from the amebas. B
• The nucleus is a cluster of granules,
with no peripheral chromatin.
• Size range 5-15 µm. This species has
no cyst stage.
105
GIARDIASIS (LAMBLIASIS)
• Etiology
– Giardia lamblia (a flagellate)
• Epidemiology
– Giardia has worldwide distribution
– It is the most frequent protozoan intestinal disease
– The most common identified cause of water-borne
disease associated with breakdown of water
purification systems, drinking from contaminated
streams, travel to endemic areas and day care
centers
106
• Giardia lamblia - a human parasite of the
gastrointestinal tract.
• The organism is spread by direct contact or
through contaminated food and water.
• Giardia spp. are pear-shaped, with hair-like
flagella for motility.
• They cause the disease giardiasis (or lambliasis),
an infection of the small intestine most
common in tropical areas.
• Giardia spp. attaches by means of sucking discs
to microvilli in the human intestine.
• Abdominal cramps, swelling, diarrhea and
nausea may occur. 107
Morphology
• Trophozoite:
– Giardia is a 12 to 15 micrometer,
– 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:
– Giardia cysts are 9 to 12 micrometer ellipsoidal cells with a
smooth well-defined wall.
– The cytoplasm contains four nuclei and many of the
structures seen in the trophozoite.
108
Giardia lamblia
A
• Cysts of Giardia lamblia,stained with
iron- hematoxylin (A, B) and in a wet
mount (C).
B
• Size: 8-12 µm in length.
• These cysts have two nuclei each (more

mature ones will have four) C
109
Giardia lamblia cyst
Giardia lamblia cyst, Iodine stain 110

Fluorescent Antibody Indirect fluorescent
(FA) Staining antibody stain
Giardia lamblia
DAPI staining Indirect fluorescent

111
of giardia antibody stain

LIFE CYCLE
• Infection occurs by ingestion of cysts, usually in
contaminated water.
• Decystation occurs in the duodenum and
• Trophozoites (trophs) colonize the upper small
intestine where they may swim freely or attach to the
sub-mucosal epithelium via the ventral suction disc.
• The free trophozoites encyst as they move down
stream and mitosis takes place during the encystment.
• The cysts are passed in the stool.
• Man is the primary host although beavers, pigs and
monkeys are also infected and serve as reservoirs.
112
LIFE CYCLE
113
Life cycle of Giardia lamblia
• Cysts are resistant forms and are responsible for
transmission of giardiasis.
• Both cysts and trophozoites can be found in the feces
(diagnostic stages).
• The cysts are hardy, can survive several months in cold
water.
• Infection occurs by the ingestion of cysts in contaminated
water, food, or by the fecal-oral route (hands or
fomites).
• In the small intestine, excystation releases trophozoites
(each cyst produces two trophozoites).
• Trophozoites multiply by longitudinal binary fission
remaining in the lumen of the proximal small bowel
where they can be free or attached to the mucosa by a
ventral sucking disk. 114
Life cycle of Giardia lamblia
• Encystation occurs as the parasites transit toward
the colon.
• The cyst is the stage found most commonly in
non-diarrheal feces .
• Because the cysts are infectious when passed in
the stool or shortly afterward, person-to-person
transmission is possible.
• While animals are infected with Giardia, their
importance as a reservoir is unclear
115
Giardia lamblia Infection in Human
G. lamblia Infection in Human Intestine

Giardia trophozoites
in section of intestine
116
SYMPTOMS
• Early symptoms include
– Flatulence (full of digestive gas),
– Abdominal distension,
– Nausea and
– Foul-smelling, bulky, explosive, often watery,
diarrhea.
– The stool contains excessive lipids but very rarely
any blood or necrotic tissue.
• The more chronic stage is associated with
– Vitamin B12 malabsorption,
– disaccharidase deficiency and
– lactose intolerance.
117
PATHOLOGY
 Covering of the intestinal epithelium by the

trophozoite and flattening of the mucosal
surface results in malabsorption of nutrients
118
IMMUNOLOGY
 There is some role for IgA and IgM and
 There is increased incidence of infection in

immunodeficient patients (e.g. AIDS).
119
DIAGNOSIS & TREATMENT
Diagnosis
• Symptoms, history, epidemiology are used in diagnosis.
• Giardia caused dysentery is distinct from other
dysenteries due to
– lack of mucus and blood in the stool,
– lack of increased PMN leukocytes in the stool and
– lack of high fever.
• Cysts in the stool and trophozoite in the duodenum can
be identified microscopically after content has been
obtained using a string device (Enterotest®).
• Trophs must be distinguished from the non-pathogenic
flagellate Trichomona hominis, which is an
asymmetrical flagellate with an undulating membrane.
Treatment
– Metronidazole is the drug of choice. 120
OTHER INTESTINAL PROTOZOA
• Balantidium coli
• Cryptosporidium parvum
• Isospora belli
 Balantidium coli and Cryptosporidium (parvum)
are both zoonotic protozoan intestinal infections
with some health significance.
 Isospora belli is an opportunistic human parasite
121
Balantidium coli
• This is a parasite primarily of cows, pigs and horses
• The organism is a large (100 x 60 micrometer) ciliate
with a macro- and a micro-nucleus.
• The infection occurs mostly in farm workers and other
rural dwellers by ingestion of cysts in fecal material of
farm animals.
• Man-to-man transmission is rare but possible
• Symptoms and pathogenesis of balantidiasis are similar
to those seen in entamebiasis, including intestinal
epithelial erosion
• However, liver, lung and brain abscesses are not seen
• Metronidazole and iodoquinol are effective
122
Balantidium coli A
Trophozoites:-
• These are characterized by their
large size (40 µm to more than 70 B
µm);
• the presence of cilia on the cell
surface - particularly visible in (B);
• a cytostome (arrows); C
• a bean shaped macronucleus which

is often visible - see (A),
• and a smaller, less conspicuous
micronucleus
123
Life cycle of B. coli
• Cysts are the parasite
stage responsible for
transmission of
balantidiasis (1)
• The host most often
acquires the cyst through
ingestion of contaminated
food or water (2)
• Following ingestion,
excystation occurs in the
small intestine, and the
trophozoites colonize the
large intestine (3)
124
Life cycle of B. coli • The trophozoites reside in the
lumen of the large intestine of
humans and animals, where
they replicate by binary fission,
during which conjugation may
occur (4)
• Trophozoites undergo
encystation to produce
infective cysts (5)
• Some trophozoites invade the
wall of the colon and multiply
• Some return to lumen and
disintegrate
• Mature cysts are passed with
feces (1)
125
Balantidium coli
126
Balantidium coli
127
Cryptosporidium parvum
• C. parvum is a small round parasite measuring 3 to 5
micrometers which is found in the gastrointestinal tract
of many animals and causes epidemics of diarrhea in
humans via contaminated food and water
• Humans are infected by ingestion of C. parvum oocysts
containing many sporozoites.
• The sporozoites are released in the upper GI tract and
attach to the gut mucosal cells where they divide to
produce merozoites.
• The merozoites invade other mucosal cells and further
multiply asexually. Some of the merozoites differentiate
into male and female gametocytes and form an oocyst
in which they multiply and differentiate into
sporozoites. The mature oocyst is excreted with fecal
material and infects other individuals
128
• When a large number of humans in a community have diarrhea,
the most likely cause is C. parvum.
• A small bolus of infection may cause mild diarrhea, whereas a
larger intake of organisms may cause more pronounced
symptoms including copious watery diarrhea, cramping
abdominal pain, flatulence and weight loss.
• Severity and duration of symptoms are related to immuno-
competence. In AIDS patients, the organism may cause prolonged,
severe diarrhea and the organisms may invade the gallbladder,
biliary tract and the lung epithelium.
• There is no approved effective treatment for cryptosporidiasis,
although paromycin is used as an investigational drug.
• There are a variety of antibody tests for detection but many of
these detect other species of Cryptosporidium than C. parvum.
• Sensitive polymerase chain reaction tests are available for C.
parvum detection in environmental and animal samples.
129
Oocysts of C.parvum stained
Oocysts of C. parvum by the acid-fast method
Oocysts of C.parvum stained

by the acid-fast method 130
131
Life cycle of Cryptosporidium
• Sporulated oocysts, containing 4 sporozoites, are excreted by
the infected host through feces and possibly other routes such
as respiratory secretions .
• Transmission of Cryptosporidium parvum occurs mainly through
contact with contaminated water (e.g., drinking or recreational
water).
• Occasionally food sources, such as chicken salad, may serve as
vehicles for transmission.
• Many outbreaks in the United States have occurred in
waterparks, community swimming pools, and day care centers.
• Zoonotic transmission of C. parvum occurs through exposure to
infected animals or exposure to water contaminated by feces of
infected animals . Following ingestion (and possibly inhalation)
by a suitable host , excystation occurs.
• The sporozoites are released and parasitize epithelial cells of the
gastrointestinal tract or other tissues such as the respiratory
tract.
132
• In these cells, the parasites undergo asexual multiplication
(schizogony or merogony) and then sexual multiplication
(gametogony) producing microgamonts (male) and
macrogamonts (female) .
• Upon fertilization of the macrogamonts by the microgametes,
oocysts develop that sporulate in the infected host.
• Two different types of oocysts are produced, the thick-walled,
which is commonly excreted from the host , and the thin-walled
oocyst , which is primarily involved in autoinfection.
• Oocysts are infective upon excretion, thus permitting direct and
immediate fecal-oral transmission.
Note that oocysts of Cyclospora cayetanensis, another
important coccidian parasite, are unsporulated at the time of
excretion and do not become infective until sporulation is
completed.
133
134
Isospora belli
• I. belli is a rare infection of normal humans, although it is
being seen in increasing numbers in AIDS patients.
• The infection occurs via the oro-fecal route. The infective
stage of the organism is an oval oocyst which, upon
ingestion, follows the same course as C. parvum.
• The disease produces symptoms similar to those of
giardiasis. In normal individuals, mild infections resolve
themselves with rest and mild diet and heavier infections
can be treated with sulpha drugs.
• The treatment may have to be carried on for a prolonged
period in AIDS patients.
135
• Oocysts of Isospora belli. The Isospora belli
oocysts are large (25 to 30 µm) and
have a typical ellipsoidal shape.
• When excreted, they are immature

and contain one sporoblast (A, B).
• The oocyst matures after excretion:

the single sporoblast divides in two
sporoblasts (C), which develop cyst
walls, becoming sporocysts, which
eventually contain four sporozoites
each.
136
Life cycle of Isospora belli
• At time of excretion, the immature oocyst contains
usually one sporoblast (more rarely two)
• In further maturation after excretion, the sporoblast
divides in two (the oocyst now contains two sporoblasts);
the sporoblasts secrete a cyst wall, thus becoming
sporocysts; and the sporocysts divide twice to produce
four sporozoites each
• Infection occurs by ingestion of sporocysts-containing
oocysts: the sporocysts excyst in the small intestine and
release their sporozoites, which invade the epithelial
cells and initiate schizogony
137
Life cycle of Isospora belli
• Upon rupture of the schizonts, the merozoites are
released, invade new epithelial cells, and continue
the cycle of asexual multiplication
• Trophozoites develop into schizonts which
contain multiple merozoites. After a minimum of
one week, the sexual stage begins with the
development of male and female gametocytes
• Fertilization results in the development of oocysts
that are excreted in the stool
• Isospora belli infects both humans and animals.
138
Life cycle of
Isospora
belli
139
LUMINAL PROTOZOA
140
TRICHOMONIASIS
Etiology
• Trichomonas vaginalis (a flagellate)
Epidemiology
• Trichomonas vaginalis has a world-wide distribution;
incidence is as low as 5% in normal females and as high
as 70% among prostitutes and prison inmates.
Morphology
• The trophozoite form is 15 to 18 micrometers in
diameter and is half pear shaped with a single nucleus,
four anterior flagella and a lateral flagellum attached by
an undulating membrane.
• Two axostyles are arranged asymmetrically. The
organism does not encyst. 141
Trichomonas vaginialis
142
TRICHOMONIASIS
Life cycle
• T. vaginalis colonizes the vagina of women and
the urethra (sometimes prostate) of men.
• Infection occurs primarily via sexual contact,
although non-venereal infections are possible.
• The organism does not encyst and divides by
binary fission which is favored by low acidity (pH >
5.9; the normal pH is 3.5 to 4.5).
• There is no non-human reservoir.
143
Life cycle
144
Symptoms & Pathology
Symptoms
• T. vaginalis infection is rarely symptomatic in men,
although it may cause mild urethritis or occasionally
prostatitis.
• In women, it is often asymptomatic, but heavy infections
in a high pH environment may cause mild to severe
vaginitis with copious foul-smelling yellowish, sometimes
frothy discharge
Pathology
• The organism causes contact-dependent damage to the
epithelium of the infected organ.
145
Trichomonas vaginalis
T. vaginalis – Vaginal discharge

146
Diagnosis
• Clinical suspicion may be confirmed by finding
the organism in Giemsa-stained smears of
vaginal discharge or, in difficult cases, by
cultivation of a swab sample in Diamond's
medium.
• Trophozoites must be distinguished from the

non-pathogenic flagellate Trichomona hominis.
147
Trichomonas vaginalis
Trichomonas – Stained vaginal secretion

148
Treatment
• Metronidazole (although teratogenic) is

effective in both males and females.
• Vinegar douche may be useful.
• Personal hygiene and the use of condoms are

helpful
149
Summary
Organism Transmission Symptoms Diagnosis Treatment
Dysentery with blood

Stool: cysts with 1-4 nuclei
Entameba and necrotic GI: Iodoquinol /Metronidazole
Oro-fecal and/or trophs.
histolytica tissue. Abscess: Metronidazole
Trophs in aspirate.
Chronic: abscesses
Fowl-smelling, bulky
Stool: typical old man
diarrhea; blood
Giardia lamblia Oro-fecal giardia troph and/or Iodoquinol / Metronidazole.
or necrotic tissue
cyst.
rare.
Dysentery with blood
Oro-fecal; and necrotic Stool: ciliated trophs and/or
Balantidium coli Iodoquinol / Metronidazole.
zoonotic tissue but no cysts.
abscesses.
Cryptosporidium
Oro-fecal Diarrhea Ooocysts in stool Paromycin (investigational)
parvum
Isospora belli Oro-fecal Giardiasis-like Ooocysts in stool Sulpha drugs
Vaginitis; occasional
Trichomonas Flagellate in vaginal (or Mebendazole; vingar douche;
Sexual urethritis/prostatit
vaginalis urethral) smear. steroids
is.
150
Trichomonas foetus
Synonym: Tritrichomonas foetus
Host: Cattle
Predilection site: Prepuce, uterus

In cows, the uterus and intermittently the
vagina.
In bulls, the preputial cavity
151
Description/Identification
The organism is pear-shaped, approximately 10-25µm
wide
Has single nucleus and four flagella, each arising from
a basal body situated in the anterior rounded end.
Three of the flagella are free anteriorly, while the 4th
extends backwards to form an undulating membrane
along the length of the organism and continues
posterioly as free flagellum
The axostyle, hyaline rod with skeletal function,
extends the length of the cell and usually projects
posteriorly
152
Morphology
153
Life cycle
The Trichomonads reproduce by longitudinal binary fission
No sexual stages are known and there are no cysts
Bulls, once infected, remain so permanently. The organisms
inhabit the preputial cavity and transmission to the cow occurs
during coitus.
From the vagina, the trichomonads reach the uterus via the
cervix to produce a low-grade endometritis. Intermittently,
organisms are flushed into the vagina, often two or three days
before oestrus
Infection is usually followed by early abortion, the organisms

being found in the amniotic and allantoic fluid
Subsequently cows appear to self-cure and, in most cases, appear

to develop a sterile immunity
154
Geographical distribution
• Worldwide: However, the prevalence has now

decresed dramatically in areas where artificial
insemination is widely practised and in
Britain, for example, the disease is now
probably extinct
155
Pathogenesis
In the bull
 Small nodules are formed on the preputial and
penile membranes shortly after infection
 The will be preputial discharge associated with the
above
 Parasites are present in small numbers in the
preputial cavity, but they concentrated in the fornix
and around the glans penis
 The chronically infected bull shows no gross lesions
156
Pathogenesis cont’d
In the cow
 The initial lesion is a vaginitis, which can be followed in animals
that become pregnant by invasion of the cervix and uterus
 Various sequelae can result, including
Placentitis leading to early abortion (1-16 weeks)
Uterine discharge
Pyometra
 Abortion before the 4th month of pregnancy is the commonest
sequel and this is normally followed by recovery
 Occasionally the developing fetal membranes are retained
leading to a purulent endometritis, a persistent utrine discharge
and anoestrus;
 Infrequently the corpus luteum is retained and the cervical seal
remains closed, when a massive pyometra devlops which visually
simulates the appearance of pregnancy
157
Pathogenesis cont’d
In some cases, despite infection, pregnancy is
not terminated by abortion and normal, full-
term calf is born
Clinical Signs:
In the bull,
– There are no clinical signs once the infecion is
established
In the cow,
Early abortion is acharacteristic feature although
this is often undetected becuase of the small size of
the fetus and the case may present as one of an
irregular oestrus cycle
158
Clinical Signs Cont’d
Other clinical signs in the cow are,
Purulent endometritis or a closed pyrometra and,
in these cases, the cow may become permanently
sterile
On the herd basis,
Cows exhibit irregular oestrous cycles, uterine
discharge, pyometra and early abortion
The cow usually recovers and generally
becomes immune, at least for that breeding
season, after infection or abortion
159
Diagnosis of Trichomonosis
Tentative diagnosis of trichomonosis is based on
The clinical history,
Signs of early abortion,
Repeated returns to service, or
Irregular oestrous cycles
Confirmation depends on demonistration of organisms
In placental fluid, aborted fetus, uterine washings, pyometra
discharge or vaginal mucus,
In the preputial washings from the bull,
The collected samples can be examined using a warm-stage
microscope for the presence of organisms
The number of organisms varies in different situations. They
are numerous in the aborted fetus, uterus and vaginal mucus
160
Diagnosis of Trichomonosis Cont’d
 The number of organisms also varies according to the
phase of oestrous cycle, being highest 3-7 days after
ovulation
 In the infected bull, T. foetus are present in highest numbers on
the mucosa of the prepuce and penis, not invading the sub-
mucosal tissues
 It is recommended to take preputial sample 1 week after the
last service. Repeat the examination on several times
 Under phase illumination it is important to see and count thre
number of flagella to differentiate T. foetus from some other
similar bovine flagellates
 Culture test (in vitro)
 Agglutination test
161
Pathology
 Infection in females causes cervicitis and endometritis leading to
infertlity, abortion or pyometra
 The inflammatory changes in the endometrium and cervix are
relatively mild and non-specific althogh there may be a copious
mucopurulent discharge
 The exudates may be continuous or intermittent in their discharge,
and the number and activity of trichomonads can vary
considerably
 Abortions may occur at any time but mainly in first half of
pregnancy
 There are no specific fetal lesions, but large numbers of protozoa
may be found in the fetal fluids and stomach
 The placenta may be covered by white or yellowish flocculent
exudates in small amounts, and thickening and haemorrhage
without necrosis may be evident on the cotyledons
 Pyometra, when it develops, may be copius with watery exudates
containing floccules which may be brownish and sticky and contain
swarms of trichomonads 162
Epidemiology
 Bulls, once infected, remain so permanently
 The trichomonads inhabit the preputial cavity and
transmission to cow occurs during coitus
 From the vagina, the parasite reach the uterus via the
cervix to produce a low-grade endometritis
 Intermittently, the parasites are flushed into the
vagina, oten 2 or 3 days before oestrus
 Infection is usually followed by early abortion, the
parasite being found in the amniotic and allantoic
fluids
 Subsequently cows appear to self-cure and in most
cases, appear to develop a sterile immunity
 Normally, one might expect the overall prevalence of
trichomonosis to be high, since it is venereally
transmitted bu bulls, which shows no clinical signs
163
Treatments
 Since the disease is self-limiting in the female
only symptomatic treatment and sexual rest for 3
months is normally necessory
 In the bull, slaughter is the best policy,
 Dimetridazole- orally or intravenously- is effective
164
Control
Artificial insemination (AI) from non-infected

donors is the only entirely satisfactory method of
control
Supervised shemes of AI is very important
165
BLOOD AND TISSUE PROTOZOA
LECTURE
3
166
• Blood protozoa of major clinical significance
include members of genera Trypanosoma
• Trypanosoma
– T. brucei and
– T. cruzi
• Leishmania
– L. donovani,
– L. tropica and
Trypanosoma cruzi
– L. braziliensis
Leishmania
167
Diseases caused by trypanosomes
• Small parasites (flagelates) that live in animals
and cause disease
• The diseases in animals are nagana/cattle,
surra/multispecies and dourine/equides
• Sleeping sickness and Chagas disease in humans is
also caused by other trypanosomes
168
• Plasmodium
– P. falciparum,
– P. ovale,
– P. malariae and
– P. vivax
• Toxoplasma gondii;
and
• Babesia
– B. microti
169
HAEMOFLAGELLATES: General Descriptions
 The haemoflagellates all belong to the family
TRYPANOSOMATIDAE, and include the
trypanosomes and leishmanias
 Trypanosomes have a leaf-like or rounded body

containing a vesicular nucleus, and a varying
number of sub-pellicular microtubules lying
beneath the outer membrane.
 There is a single flagellum arising from a
kinetosome or basal body or granule
 An undulating membrane is present and the
flagellum lies on its outer border
170
Morphology Cont’d
• Posterior to the kinetosome is a rod-shaped or
spherical kinetoplast containing DNA.
• Members of this family were originally parasites
of the intestinal tract of insects, and many are still
found in insects.
• Others are heteroxenous, spending part of their
life cycle in a vertebrate host and part in an
invertebrate host.
• Trypanosomes have been around for more than
300 million years. They are parasites of insects,
plants, birds, bats, fish, amphibians and mammals
171
MORPHOLOGY cont’d
• Trypanosomes are actively motile flagellated
parasites that live in the blood and lymph
• Members of the genus Trypanosoma are
heteroxenous and pass through amastigote,
promastigote, epimastigote and tryptomastigote
stages in their life cycle.
• In some species only tryptomastigote forms are
found in the vertebrate host; in others,
presumably more primitive species, both
amastigote and tryptomastigote forms are
present. 172
MORPHOLOGY cont’d
• In the amastigote form, the body is rounded and the
flagellum emerges from the body through a wide,
funnel-shaped reservoir.
• In the promastigote form, the kinetoplast and
kinetosome are anterior in the body and there is no
undulating membrane.
• In the epimastigote form, the kinetoplast and
kinetosome are just posterior to the nucleus and the
undulating membrane runs forward from there.
• In the tryptomastigote form, the kinetoplast and
kinetosome are near the posterior end and the flagellum
forms the border of an undulating membrane that
extends along the side of the body to the anterior end.
173
Example, MORPHOLOGY T. brucei brucei
• Amastigote - Basal body
anterior of nucleus, with a
short, essentially non-
functional, flagellum.
• Promastigote - Basal body
anterior of nucleus, with a long
detached flagellum.
• Epimastigote - Basal body
anterior of nucleus, with a long
flagellum attached along the
cell body.
• Trypomastigote - Basal body
posterior of nucleus, with a
long flagellum attached along
the cell body.
174
THE TRANSMISSION OF TRYPANOSOME INFECTION IN ANIMALS
• With one exception, all trypanosomes have arthropod vectors in
which transmission is either cyclical or non-cyclical.
• In cyclical transmission the arthropod is a necessary intermediate

host, in which the trypanosomes multiply, undergoing a series of
morphological transformations before forms infective for the next
mammalian host are produced.
• When multiplication occurs in the digestive tract and proboscis, so
that the new infection is transmitted when feeding, the process is
known as anterior station development: the various species of
trypanosomes which use this process are often considered as a
group, the Salivaria. All are trypanosomes transmitted by tsetse
flies, the main species being Trypanosoma congolense (subgenus
Nanomonas). T. vivax (subgenus Duttonella) and T. brucei
(subgenus Trypanozoon).
175
Posterior station development
• In other trypanosomes, multiplication and
transformation occurs in the gut and the infective
forms migrate to the rectum and are passed with the
faeces; this is posterior station development and the
trypanosome species are grouped together as the
Stercoraria.
• In domestic animals, these are all relatively non-
pathogenic trypanosomes such as Trypanosoma
theileri and T. melophagium transmitted by tabanid
flies and sheep keds respectively.
• This is certainly not the case in man in which T. cruzi,
the cause of the serious Chagas’ disease in South
America, is transmitted in the faeces of reduviid bugs.
176
Non-cyclical transmission
• Is essentially mechanical transmission in which the trypanosomes are
transferred from one mammalian host to another by the interrupted feeding
of biting insects, notably tabanids and Stomoxys.
• The trypanosomes in or on the contaminated proboscis do not multiply and

die quickly so that cross-transmission is only possible for a few hours.
• Trypanosoma evansi, widely distributed in livestock in Africa and Asia, is

transmitted mechanically by biting flies.
• However, in Central and South America, T. evansi is also transmitted by the

bites of vampire bats in which the parasites are capable of multiplying and
surviving for a long period.
• Strictly speaking, this is more than mere mechanical transmission, since the
bat is also a host, although it is certainly non-cyclical, since the multiplying
trypanosomes in the bat’s blood do not undergo any morphological
transformation before they migrate into the buccal cavity.
177
Tsetse flies
• Tsetse flies belong to subgenus Glossina, contains a total of
seven species and sub-species
• Those of major economic importance are G. morsitans and G.
pallidipes
• Species of the Glossina sub-genus are called the savannah
flies due to their preference for this environment.
178
Note
• It is important to note that the Salivarian trypanosomes, normally
transmitted cyclically in tsetse flies, may on occasions be
transmitted mechanically. E.g. T. vivax can be transmitted
mechanically by biting flies
• Apart from classical cyclical and non-cyclical transmission, dogs,
cats and wild carnivores may become infected by eating fresh
carcasses or organs of animals that have died of trypanosomosis,
the parasites penetrating oral abrasions (rubbing or scraping away
of layer of cells or tissue)
• The important trypanosome infections of domestic animals
differ considerably in many respects and are best treated
separetly.
• The African species responsible for the tsetse-transmitted
trypanosomoses, i.e., Salivaria, are generally considered to be the
most significant
179
TRYPANOSOMIOSIS
Members of the genus Trypanosoma are
haemoflagellates of overwhelming importance in cattle
in sub-Saharan Africa as a cause of trypanosomiosis
Salivarian trypanosomes
A number of species of Trypanosoma, found in domestic
and wild animals, are all transmitted cyclically by
Glossina in much of sub-Saharan Africa
The disease, sometimes known as nagana, characterized
by lymphadenopathy and anaemia accompanied by
progressive emaciation and, often, death
180
PATHOGENESIS
The signs and effects of the various trypanosomes
found in domestic animals are more or less similar. The
pathogenesis of trypanosomosis may be considered
under three headings:
1. Lymphoid Enlargement and Splenomegaly
 Develop associated with plasma cell hyperplasia and
hypergammaglobulinaemia, which is primarily due to
an increase in IgM
 Concurrently there is a variable degree of suppression
of immune responses to other antigens such as
microbial pathogens or vaccines
 In infections of long duration, the lymphoid organs and
spleen become shrunken due to exhaustion of their
cellular elements
181
2. Anaemia
 Is a cardinal feature of the disease, particularly in cattle, and
initially is proportional to the degree of parasitemia
 Anaemia is caused mainly by extravascular haemolysis through
erythrophagocytosis in the mononuclear phagocytic systems of the
spleen, liver and lungs, but as the disease becomes chronic there
may be decreased haemoglobine synthesis
 Leucopenia and thrombocytopenia are caused by mechanisms that
predispose leucocytes and platelets to phagocytosis
 Immunological mechanisms in the pathogenesis lead to extensive
proliferation of activated macrophages, which engulf or destroy
erythrocytes, leucocytes, platelets and haematopoietic cells
 Later, in infections of several months´ duration, when the
parasitaemia often becomes low and intermittent, the anaemia
may resolve to a variable degree. However, in some chronic cases
it may persist despite chemotherapy
182
3. Cell Degeneration and Inflammatory Infiltrates
 Occur in many organs, such as the skeletal muscle

and the central nervous system, but perhaps most
significantly in the myocardium where there is
separetion and degenaration of the muscle fibres
 The mechanisms underlying these changes are

still under study
183
CLINICAL SIGNS
In cattle, the major signs are
• Anaemia,
• Generalised enlargement of the superficial lymph glands,
• Lethargy and progressive loss of body condition.
• Fever and loss of appetite occur intermittently during
parasitaemic peaks, the later becoming marked in the
terminal stages of the disease
• The disease is chronic, extending over several months,
and usually terminates fatally if untreated
• As a herd phenomenon, the growth of young animals is
stunted, while adults show decreased fertility, and if
pregnant, may abort or give birth too weak offspring
184
CLINICAL SIGNS Cont’d
In the terminal stages, animals become extremely
weak, the lymph nodes are reduced in size and
there is often a jugular pulse.
Death is associated with congestive heart failure
due to anaemia and myocarditis.
Occasionally, the disease is acute, death occuring
within 2-3 weeks of infection preceded by fever,
anaemia and widespread haemorrhages
185
PATHOLOGY OF ANIMAL TRYPANOSOMOSES
 Trypanosomoses are usually chronic disorders, the duration and
symptoms of which vary with the animal host species and the
pathogen
 Three disease groups can be distinguished
1. Nagana: diseases due to African trypanosomes (T. vivax, T.
uniforme, T. congolense, T. simiae, T. brucei, T. suis) are all
cyclically transmitted by the tsetse fly
2. Surra, a trypanosomosis of Camelidae and equines due to T.
evansi, is transmitted by biting insects other than tsetse flies (as
horseflies). A severe febrile and hemorrhagic disease marked by
edema and anemia, commonly fatal in horses, mules, and camels
although cattle and dogs often recover
3. Dourine is a contagious trypanosomosis of equine, due to T.
equiperdum, transmitted from host to host during copulation
and chronic course marked by inflammation of the genitals,
subcutaneous edematous plaques, low-grade fever, progressive
paralysis, emaciation, and death
186
African Trypanosomosis of Domestic Animals
General symptoms
 After an incubation period that may vary from a few weeks to a
few months, these diseases are generally characterized by bouts
of fever with intermittent apyrexia, changes in the blood with
anaemia, oedema, splenomegaly and polyadenities, nervous
disorders and with paresis of the hind limbs, pica, eye disorders,
emaciation leading to cachexia and death
Hyperpyrexia
 Disease attacks are usually accompanied by hyperpyrexia. The
presence of a large number of trypanosomes in the blood causes
the temperature to rise to over 40oC.
 High parasitaemia and hyperthermia occurs intermittently in a
serious of frequent attacks
 In acute cases, the attacks are few but at short intervals, resulting
in rapid death. They are less severe and less frequent in the
chronic forms
187
Anaemia
 The severity of this condition depends on disease developmental
stage, but it is always more acute in the terminal stages.
 It may be very acute in chronic forms accompanied by cachexia.
 It is, however, less rapid and acute compared with piroplasmoses.
 Anaemia is sometimes accompanied by icterus, especially in dogs
Oedemas
 Oedemas are frequent and usually in the lower part of the belly
and genital organs
 They often begin in the form of an oedematous swelling, situated
in the median part of the thoracoabdominal wall, and gradually
extend to the limbs
188
Splenomegaly and polyadenitis
 Splenomegaly is generally present, but its severity varies
with the animal species; although very severe in dogs, it
is not marked in cattle and goats.
 A high trypanosome density and prolonged infection
aggravate this condition
 Adenitis is very common. In man, one of the first signs is
adenitis of the neck glands.
 In animals, hypertrophy occurs in the inguinal, and
precrural lymph nodes
Nervous and ocular disorders
 Disorders of the nervous system vary in nature and
dominate the 2nd stage of disease development in man
 The 1st symptoms are irritability, hyperesthesia,
insomnia, leading to somnolence, coma and paralysis
189
 In animals, the signs are weakness of the hind quarters,
occasionally paresis or paralysis shortly before death
 Vision difficulties are frequent and characterized by opaqueness of
the cornea, and in horses and dogs, by interstitial keratitis (uveitis)
 An occasionally purulent form of conjunctivitis may also occur
Emaciation
 Emaciation is a regular symptom in the advanced stages of the
disease
 The digestive system usually functions normally
 Emaciation is more acute when the disease develops slowly.
 Sometimes diarrhoea can cause intense intestinal evacuation
 Inthe terminal phase, the animal dies in a state of advanced
cachexia
Apart from these main symptomes, abortions and drying up of
milk secretion in females are often observed in chronic cases as
well as sterility in males and growth retardation in the young. Draft
animals are found to be slow at work
190
PATHOLOGY
 The carcass is often pale, emaciated and there may be
oedematous swellings in the lower part of the abdomen
and genital organs with serous atrophy of fat
 The liver, lymph nodes and spleen are enlarged and the
viscera are congested
 Petechiae may appear on lymph nodes, pericardium and
intestinal mucosa
 The liver is hypertrophic and congested with
degeneration, necrosis of the hepatocytes, dilation of
blood vessels and parenchymal infiltration of
mononuclear cells
 A non-suppurative myocarditis, sometimes associated
with hydropericarditis, has been reported accompanied
by degeneration and necrosis of the myocardial tissue
191
PATHOLOGY Cont’d
Other lesions are:
 Glomerulonephritis,
 Renal tubular necrosis,
 Non-suppurative meningio-encephalomyelitis,
 Focal poliomalacia,
 Keratitis,
 Opthalmitis,
 Orchitis,
 Intestinal pneumonia and
 Bone marrow atrophy
 Splenic and lymph node hypertrophy occur during the
acute phase
 But the lymphoid tissues are usually exhausted and
fibrotic in the chronic stage
192
DIAGNOSIS
 The clinical signs of the disease, although indicative, are not
pathognomonic symptoms (specially, distinctively, or decisively
characteristic of a particular disease)
 Confirmation of clinical diagnosis depends on the demonstration
of trypanosomes in the blood
 If a herd or flock is involved, representative number of blood
samples should be examined
 Occasionally, when the parasitaemia is massive it is possible to
detect motile trypanosomes in fersh films of blood
 Both thick and thin smears of blood are air-dried and examined
later
 Thick smears, de-haemoglobinised before staining with Giemsa or
Leishman’s stain, offer a better chance of finding trypanosomes
 While stained thin smears are used for differentiation of the
trypanosome species
193
DIAGNOSIS Cont’d
 More sensitive techniques utilise centrifugation in a
microhaematocrit tube followed by microscopic
examination of the interface between the buffy coat and
the plasma;
 Alternatively, the tube may be snapped, the buffy coat
expressed on to a slide, and the contents examined
under dark-ground or phase-contrast microscopy for
motile trypanosomes
 Packed red cell volume (PCV) is also obtained with these
technique
 A numbers of serological tests have been described and
include indirect fluorescent antibody test (IFAT) and
ELISA and have been partially validated but require
further evaluation and standardisation
194
EPIDEMIOLOGY
 The vectors are various species of Glossina including G.
morsitans, G. palpalis, G. longipalpes and G. austeni.
 T. congolense can also be transmitted mechanically by
other biting flies in tsetse-free areas, although this is
uncommon
 Since the life cycle of T. vivax is short, it is more readily
transmitted than other species and mechanical
transmission of T. vivax by tabanids allows it to spread
outside the tsetse belt.
 The disease can also be transmitted mechanically
through contaminated needles and instruments
195
The epidemiology depends on three factors: the
distribution of the vectors(tsetse flies, and other biting
flies), virulence of the parasite and the response of the
host (domestic or wild mammals)
1. The Vectors:
 Of the three groups of tsetse flies, the savannah and
riverine are the most important since they inhabit areas
suitable for grazing and watering
 Although the infection rate of Glossina with
trypanosomes is usually low, ranging from 1-20% of the
flies, each is infected for life, and their presence in any
number makes the rearing of cattle, pigs and horses
extremely difficult
 Biting flies may act as mechanical vectors, but their
significance in Africa is still undefined
196
2. The Parasite:
 Since parasitaemic animals commonly survive for
prolonged periods, there are ample opportunities
for fly transmission
 The most important aspects of trypanosomosis
which accounts for the persistant parasitaemia is
the way in which the parasite evades the immune
reponse of the host
 The metacyclic and bloodstream trypanosomes
possess a glycoprotein coat which is antigenic and
provokes the formation of antibodies which cause
opsonisation and lysis of the trypanosomes
197
3. The host:
 Trypanosomosis is basically an infection of wildlife
that are parasitaemic for prolonged periods, but
generally remain in good health
 This situation is known as trypanotolerance
198
 Unfortunately, by the time the antibody is produced, a
proportion of the trypanosomes have altered the
composition of their glycoprotein coat and now, displying
a different antigenic surface, are unaffected by the
antibody.
 Those trypanosomes possessing this new variant antigen
multiply to produce a 2nd wave of parasitaemia
 The host produce a 2nd antibody, but again the
glycoprotein coat has altered in a number of
trypanosomes so that a 3rd wave of parasitaemia occurs
 This process of antigenic varation associated with waves
and remissions of parasitaemias, often at weakly
intervales, may continue for months, usually with a fatal
outcome
199
African Animal Trypanosomosis (AAT)
T. congolense = most common species
T. vivax - also in the Western Hemisphere
T. brucei (b. brucei, b. rhodiense*, b. gambiense*)
[T. evansi = sexually tranmitted]
• Wild & domestic mammals + humans*

• Southern edge of the Sahara desert to Angola,
Zimbabwe, and Mozambique
• Most important in cattle and humans
• Spread by tsetse fly “destroy cattle”
• Carriers (often wildlife)
• Trypanosomes replicate in the tsetse fly
• Transmitted cyclically through tsetse fly saliva
– Glossina morsitans open woodland of the savanna
– G. palpalis shaded habitat adjacent to rivers and lakes
– G. fusca high, dense forest areas
• Also mechanically transmitted by flies of the genus
Tabanus, Stomoxys, Chrysops etc
200
African Animal Trypanosomosis (AAT)
Pathogenesis and Clinical signs
Nagana “to be in low or depressed spirits”
• Anemia
• Lymphoid enlargement and spleneomegaly
• Cell degeneration and inflammatory infiltrates in the
myocaridium
VSG variant surface glycoprotein
201
Trypanotolerance
the capacity of an animal to control the
development of the parasites and to limit their
pathological effects, i.e. anaemia
202
Control
Control of Trypanosomosis depends on
 The epidemiology of the disease (parasites, hosts and
vectors)
 Control of the tsetse flies
 Treatments
• Treatment with a trypanocidal drug at an appropriate time is
advisable
• The trypanocidal drugs are belonging to four chemical families
• Suramin (suramin sodium), a urea compound
• Ethidium (homidium bromide), Novidium, Prothidium
(pyrithidium bromide), Trypamidium or Samorin
(isometamidium), all phenanthridinium compounds
• Trypacide sulphate and Trypacide prosalt,
quinapyramine compounds
• Berenil (diminazene aceturate), an aromatic amidine
compound
203
Drug Recommended dose Comments
Diminazine 3-10 Mg/Kg, i.m. T. brucei,
aceturate T. congolense
T. vivax
Isometamidium 0.25 – 1 Mg/Kg, i.m. T. brucei,
T. congolense
T. vivax
Local reaction
Homidium bromide 1 Mg/Kg, s.c T. congolense,
T. vivax
Homidium chloride Prophylaxis for 6
weeks
Pyrithidium bromide 2 – 2.5 Mg/Kg T. congolense,
T. vivax
Prophylaxis for 4
months 204
• In cattle, sheep and goats, Isometamidium is the drug
of choice since it remains in the tissues and has a
prophylactic effects for 2-6 months
 Vaccines
• Killed or irradiated trypanosomes have given promising
results in laboratory animals, but not reliable in the field
• Virulent trypanosome strains, then treating with drugs, but
not successful due to multiplicity of serotypes
 Using trypanotolerant breeds of ruminants
• Combined with judicious drug therapy may be a realistic
solutions
205
Vector Control
 Trypanosomosis vector control campaigns are
mainly directed against steste flies, the most
important vectors of the disease
 Although their radication in a given area may be
considered as the ideal solution to the
trypanosomosis problem, it is effective only when
supplemented by trypanocidal treatments
 Tsetse fly control campaigns are based on the use
of insecticides (ground spray application or aerial
spraying from helicopters)
206
Vector Control cont’d
Biological Control
 It is still at experimental stage
Genetic Control (Autocidal OR Autodestruction)

 Release of sterile males (When a femele is insimenated with male
previously exposed to gamma rays, the spermatozoid
chromosomes are dameged by the rays and fail to pair up with
those of the ovules. Embryogenesis is blocked and the female can
no longer reproduce)
 Sterrilizing agents used are
• Alcoylants
• Ionizing radiations (X-rays, gamma rays, neutrons)
 It is very specific
 Non-pollutant
 Has no adverse effects on other animals
207
AFRICAN TRYPANOSOMIASIS (SLEEPING
SICKNESS)
Etiology
– There are two clinical forms of African
trypanosomiasis:
1. a slowly developing disease caused by
Trypanosoma brucei gambiense and
2. a rapidly progressing disease caused by

T. brucei rhodesiense
208
AFRICAN TRYPANOSOMIASIS (SLEEPING
SICKNESS)
Epidemiology
• T. b. gambiense is predominant in the western
and central regions of Africa,
• Whereas T. b. rhodesiense is restricted to the
eastern third of the continent.
• 6,000 to 10,000 human cases are documented
annually.
• 35 million people and 25 million cattle are at risk.
• Regional epidemics of the disease are cause of
major health and economic disasters.
209
DISTRIBUTION OF AFRICAN TRYPANOSOMIASIS
• Distribution of West
African or Gambian
Sleeping Sickness and
• Distribution of East
African or Rhodesian
Sleeping Sickness
210
AFRICAN TRYPANOSOMIASIS
Morphology
• T. b. gambiense and T. b. rhodesiense are similar
in appearance
• The organism measures 10 - 30 micrometers X 1-
3 micrometers.
• It has a single central nucleus and a single
flagellum originating at the kinetoplast and joined
to the body by an undulating membrane
• The outer surface of the organism is densely
coated with a layer of glycoprotein, the variable
surface glycoprotein (VSG)
211
MORPHOLOGY • Thin blood smear stained with
Giemsa.
• Typical trypomastigote stages

(the only stages found in
patients), with a posterior
kinetoplast, a centrally located
nucleus, an undulating
membrane, and an anterior
flagellum.
212
MORPHOLOGY • The two Trypanosoma
brucei species that cause
human trypanosomiasis, T.
b. gambiense and T. b.
rhodesiense, are
undistinguishable
morphologically.
• The trypanosomes length

range is 14-33 µm
213
MORPHOLOGY
• During a blood meal on the mammalian host, an
infected tsetse fly (genus Glossina) injects metacyclic
trypomastigotes into skin tissue.
• The parasites enter the lymphatic system and pass into
the bloodstream
• Inside the host, they transform into bloodstream
trypomastigotes , are carried to other sites throughout
the body, reach other blood fluids (e.g., lymph, spinal
fluid), and continue the replication by binary fission
• The entire life cycle of African Trypanosomes is
represented by extracellular stages.
• The tsetse fly becomes infected with bloodstream
trypomastigotes when taking a blood meal on an
infected mammalian host
214
MORPHOLOGY
• In the fly’s midgut, the parasites transform into
procyclic trypomastigotes, multiply by binary
fission , leave the midgut, and transform into
epimastigotes
• The epimastigotes reach the fly’s salivary glands
and continue multiplication by binary fission
• The cycle in the fly takes approximately 3 weeks.
Humans are the main reservoir for Trypanosoma
brucei gambiense, but this species can also be
found in animals.
• Wild game animals are the main reservoir of T. b.
rhodesiense. 215
Different Forms/Life Stages
216
LIFE CYCLE
• The infective, metacyclic form of the trypanosome is
injected into the primary host during a bite by the
vector, the tsetse fly
• The organism transforms into a dividing trypanosomal
(trypomastigote) blood form as it enters the draining
lymphatic and blood stream.
• The trypanosomal form enters the vector during the
blood meal and travels through the alimentary canal
to the salivary gland where it proliferates as the
crithidial form (epimastigote) and matures to
infectious metacyclic forms
217
LIFE CYCLE
• Trypomastigotes can traverse the walls of blood
and lymph capillaries into the connective
tissues and, at a later stage, cross the choroid
plexus into the brain and cerebrospinal fluid.
• The organism can be transmitted through blood
transfusion.
218
219
SYMPTOMS
• The clinical features of Gambian and Rhodesian disease
are the same, however they vary in severity and
duration.
• Rhodesian disease progresses more rapidly and the
symptoms are often more pronounced.
• The symptoms of the two diseases are also more
pronounced in Caucasians than in the local African
population.
• Classically, the progression of African trypanosomiasis
can be divided into three stages: the bite reaction
(chancre), parasitemia (blood and lymphoid tissues), and
CNS stage.
• Bite reaction: A non-pustular, painful, itchy chancre
forms 1-3 weeks after the bite and lasts 1-2 weeks. It
leaves no scar.
220
SYMPTOMS
• Parasitemia: Parasitemia and lymph node invasion is
marked by attacks of fever which starts 2-3 weeks after
the bite and is accompanied by malaise, lassitude,
insomnia headache and lymphadenopathy and edema
• Painful sensitivity of palms and ulnar region to pressure
(Kerandel's sign) may develop in some Caucasians.
• Very characteristic of Gambian disease is visible
enlargement of the glands of the posterior cervical
region (Winterbottom's sign)
• Febrile episodes may last few months as in Rhodesian
disease or several years as in Gambian disease.
• Parasitemia is more prominent during the acute stage
than during the recurrence episodes.
221
SYMPTOMS
• CNS Stage: The late or CNS stage is marked by changes
in character and personality.
• They include lack of interest and disinclination to work,
avoidance of acquaintances, morose and melancholic
attitude alternating with exaltation, mental retardation
and lethargy, low and tremulous speech, tremors of
tongue and limbs, slow and shuffling gait, altered
reflexes, etc.
• Males become impotent. There is a slow progressive
involvement of cardiac tissue.
• The later stages are characterized by drowsiness and
uncontrollable urge to sleep. The terminal stage is
marked by wasting and emaciation.
• Death results from coma, intercurrent infection or
cardiac failure 222
SYMPTOMS
223
PATHOLOGY AND IMMUNOLOGY
• An exact pathogenesis of sleeping sickness is not known,

although immune complexes and inflammation have
been suspected to be the mechanism of damage to
tissues.
• The immune response against the organism does help
to eliminate the parasite but it is not protective, since
the parasite has a unique ability of altering its antigens,
the VSG (see the chapter on
Molecular Biology of Trypanosomes).
• Consequently, there is a cyclic fluctuation in the number
of parasites in blood and lymphatic fluids and each wave
of parasite represents a different antigenic variant.
224
• The parasite causes polyclonal expansion of B

lymphocytes and plasma cells and an increase in
total IgM concentration.
• It stimulates the reticuloendothelial function. It
also causes severe depression of cell mediated
and humoral immunity to other antigens.
225
NEUROPATHOLOGY OF HUMAN AFRICAN
TRYPANOSOMIASIS
226
DIAGNOSIS
• Detection of parasite in the bloodstream, lymph
secretions and enlarged lymph node aspirate
provides a definitive diagnosis in early (acute)
stages.
• The parasite in blood can be concentrated by
centrifugation or by the use of anionic support
media.
• Cerebrospinal fluid must always be examined for
organisms. Immuno-serology (enzyme-linked
immune assay, immunofluorescence) may be
indicative but does not provide definite diagnosis.
227
TREATMENT AND CONTROL
• The blood stage of African trypanosomiasis can be
treated with reasonable success with Pentamidine
isethionate or Suramin.
• These drugs have been reported also to be effective in
prophylaxis although they may mask early infection and
thus increase the risk of CNS disease.
• Cases with CNS involvement should be treated with
Melarsoprol, an organic arsenic compound.
• The most effective means of prevention is to avoid
contact with tsetse flies.
• Vector eradication is impractical due to the vast area
involved.
• Immunization has not been effective due to antigenic
variation.
228
American Trypanosomosis
• Trypanosoma cruzi
• In humans Chagas disease
• In rural areas
• All mammals may be infected
(especially opposums,
raccoons, rodents, cats and
dogs)
• The vectors are reduvidae
bugs which are
haematophagous and the most
important are Triatoma
infestans
Southern cone initiative
229
AMERICAN TRYPANOSOMIASIS (CHAGAS'
DISEASE)
Etiology
• Chagas' disease is caused by the protozoan
hemoflagellate, Trypanosoma cruzi
230
CHAGAS' DISEASE
Epidemiology
• American trypanosomiasis, also known as Chagas'
disease, is scattered irregularly in Central and South
America, stretching from parts of Mexico to Argentina
(figure ).
• Rare cases have been reported in Texas, California and
Maryland.
• It is estimated that 16-18 million people are infected by
the parasite and 50 million are at risk.
• About 50,000 people die each year from the disease.
231
Chagas Disease Distribution Map
• Figure 6.
Chaga's
disease:
Countries in
which
American
trypanosom
iasis is
endemic.
WHO
232
CHAGAS' DISEASE
Morphology
• Depending on its host environment, the organism
occurs in three different forms (Figure 7).
• The trypanosomal (trypomastigote) form (figure 7A),
found in mammalian blood, is 15 to 20 microns long and
morphologically similar to African trypanosomes.
• The crithidial (epimastigote) form (figure 7B) is found in
the insect intestine.
• The leishmanial (amastigote) form (figure 7C), found
intracellularly or in pseudocysts in mammalian viscera
(particularly in myocardium and brain), is round or oval
in shape, measures 2-4 microns and lacks a prominent
flagellum.
233
Morphology A
• Figure 7A
Trypanosoma cruzi,
trypomastigote form, in a
blood smear (Giemsa B
stain)
• Figure 7B Trypanosoma
cruzi, crithidia.
• Figure 7C. Trypanosoma
cruzi. Leishmanial form
C
234
LIFE CYCLE
• The organism is transmitted to mammalian host by many
species of kissing (riduvid) bug (figure 8), most
prominently by Triatoma infestans, T. sordida,
Panstrongylus megistus and Rhodnius prolixus.
• Transmission takes place during the feeding of the bug
which normally bites in the facial area (hence the name,
kissing bug) and has the habit of defecating during
feeding.
• The metacyclic trypamastigotes, contained in the fecal
material, gain access to the mammalian tissue through
the wound which is often rubbed by the individual that is
bitten.
235
Kissing Bug
• Figure 8 Riduvid bug,

the vector of American
trypanosomiasis
236
LIFE CYCLE
• Subsequently, they enter various cells,
including macrophages, where they
differentiate into amastigotes and multiply by
binary fission.
• The amastigotes differentiate into non-
replicating trypomastigotes and the cells
rupture to release them into the bloodstream.
• Additional host cells, of a variety of types, can
become infected and the trypomastigotes
once again form amastigotes inside these
cells.
237
LIFE CYCLE
• Uninfected insect vectors acquire the
organism when they feed on infected animals
or people containing trypomastigotes
circulating in their blood.
• Inside the alimentary tract of the insect

vector, the trypomastigotes differentiate to
form epimastigotes and divide longitudinally
in the mid and hindgut of the insect where
they develop into infective metacyclic
trypomastigotes (figure 9C).
238
LIFE CYCLE
• Transmission may also occur from man to
man by blood transfusion and by the
transplacental route
• More than one hundred mammalian species

of wild and domestic animals including cattle,
pigs, cats, dogs, rats, armadillo, raccoon and
opossum are naturally infected by T. cruzi and
serve as a reservoir.
239
Life Cycle 240
Life Cycle
• An infected triatomine insect vector (or “kissing” bug) takes a
blood meal and releases trypomastigotes in its feces near the site
of the bite wound.
• Trypomastigotes enter the host through the wound or through
intact mucosal membranes, such as the conjunctiva
• Common triatomine vector species for trypanosomiasis belong to
the genera Triatoma, Rhodinius, and Panstrongylus.
• Inside the host, the trypomastigotes invade cells, where they
differentiate into intracellular amastigotes .
• The amastigotes multiply by binary fission and differentiate into
trypomastigotes, and then are released into the circulation as
bloodstream trypomastigotes
• Trypomastigotes infect cells from a variety of tissues and
transform into intracellular amastigotes in new infection sites.
241
Life Cycle
• Clinical manifestations can result from this infective cycle. The
bloodstream trypomastigotes do not replicate (different from the
African trypanosomes).
• Replication resumes only when the parasites enter another cell or
are ingested by another vector.
• The “kissing” bug becomes infected by feeding on human or
animal blood that contains circulating parasites .
• The ingested trypomastigotes transform into epimastigotes in the
vector’s midgut. The parasites multiply and differentiate in the
midgut and differentiate into infective metacyclic
trypomastigotes in the hindgut
• Trypanosoma cruzi can also be transmitted through blood
transfusions, organ transplantation, transplacentally, and in
laboratory accidents.
242
Symptoms
• Chagas' disease can be divided into three
stages: the primary lesion, the acute stage,
and the chronic stage.
• The primary lesion, chagoma, appearing at the
site of infection, within a few hours of a bite,
consists of a slightly raised, flat non-purulent
erythematous plaque surrounded by a
variable area of hard edema.
• It is usually found on the face, eyelids, cheek,
lips or the conjunctiva, but may occur on the
abdomen or limbs.
243
Symptoms
• When the primary chagoma is on the face,
there is an enlargement of the pre- and post-
auricular and the submaxillary glands on the
side of the bite.
• Infection in the eyelid, resulting in a unilateral

conjunctivitis and orbital edema (Ramana's
sign) (figure 9A), is the commonest finding.
244
Symptoms
• Figure 9A Ramana's
sign: unilateral
conjunctivitis and
orbital edema
245
Symptoms: Acute Stage
• The acute stage appears 7-14 days after infection.
• It is characterized by restlessness, sleeplessness,
malaise, increasing exhaustion, chills, fever and
bone and muscle pains.
• Other manifestations of the acute phase are
cervical, axillary and iliac adenitis, hepatomegaly,
erythematous rash and acute myocarditis.
• There is a general edematous reaction associated
with lymphadenopathy.
246
Symptoms: Acute Stage
• Diffuse myocarditis, sometimes accompanied by
serious pericarditis and endocarditis, is very
frequent during the initial stage of the disease.
• In children, Chagas' disease may cause meningo-
encephalitis and coma.
• Death occurs in 5-10 percent of infants.
Hematologic examination reveals lymphocytosis
and parasitemia.
247
Symptoms: Chronic Stage
• The acute stage is usually not recognized and
often resolves with little or no immediate
damage and the infected host remains an
asymptomatic carrier.
• An unknown proportion (guessed at 10-20%) of
victims develop a chronic disease.
• They alternate between asymptomatic remission
periods and relapses characterized by symptoms
seen in the acute phase.
• Cardiac arrhythmia is common.
248
• The chronic disease results in an abnormal
function of the hollow organs, particularly the
heart, esophagus and colon.
• The cardiac changes include myocardial
insufficiency, cardiomegaly, disturbances of atrio-
ventricular conduction and the Adams-Stoke
syndrome.
• Disturbances of peristalsis lead to
megaesophagus and megacolon (figure 9B).
249
• Figure 9B Megacolon in
Chaga's disease
250
• The pathological effects of acute phase Chagas' disease
largely result from direct damage to infected cells.
• In later stages, the destruction of the autonomic nerve
ganglions may be of significance.
• Immune mechanisms, both cell mediated and humoral,
involving reaction to the organism and to autologous
tissues have been implicated in pathogenesis.
• T. cruzi stimulates both humoral and cell mediated
immune responses.
• Antibody has been shown to lyze the organism, but
rarely causes eradication of the organism, perhaps due
to its intracellular localization. 251
• Cell mediated immunity may be of significant value.
While normal macrophages are targeted by the
organism for growth, activated macrophages can kill the
organism.
• Unlike T. brucei, T. cruzi does not alter its antigenic coat.
• Antibodies directed against heart and muscle cells have
also been detected in infected patients leading to the
supposition that there is an element of autoimmune
reaction in the pathogenesis of Chagas' disease.
• The infection causes severe depression of both cell
mediated and humoral immune responses.
• Immunosuppression may be due to induction of
suppressor T-cells and/or overstimulation of
macrophages.
252
DIAGNOSIS
• Clinical diagnosis is usually easy among children in
endemic areas.
• Cardiac dilation, megacolon and megaesophagus in
individuals from endemic areas indicate present or
former infection.
• Definitive diagnosis requires the demonstration of
trypanosomes by microscopy or biological tests (in the
insect or mice).
• Antibodies are often detectable by complement fixation
or immunofluorescence and provide presumptive
diagnosis.
253
• There is no curative therapy available.
• Most drugs are either ineffective or highly toxic.
• Recently two experimental drugs, Benznidazol and
Nifurtimox have been used with promising results in the
acute stage of the disease, however their side effects
limit their prolonged use in chronic cases.
• Control measures are limited to those that reduce
contact between the vectors and man.
• Attempts to develop a vaccine have not been very
successful, although they may be feasible.
254
LEISHMANIASIS
Etiology
• Several species of Leishmania are pathogenic for man:
• L. donovani causes visceral leishmaniasis (Kala-azar,
black disease, dumdum fever);
• L. tropica (L. t. major, L. t. minor and L. ethiopica)
cause cutaneous leishmaniasis (oriental sore, Delhi
ulcer, Aleppo, Delhi or Baghdad boil); and
• L. braziliensis (also, L. mexicana and L. peruviana) are
etiologic agents of mucocutaneous leishmaniasis
(espundia, Uta, chiclero ulcer)
255
LEISHMANIASIS
Epidemiology:-
• Leishmaniasis is prevalent world wide:
ranging from south east Asia, Indo-
Pakistan, Mediterranean, north and
central Africa, and south and central
America.
256
LEISHMANIASIS
Morphology:-
• Amastigote (leishmanial form) is oval and measures 2-5

microns by 1 - 3 microns (figure 10A-D),
• Whereas the leptomonad measures 14 - 20 microns by

1.5 - 4 microns, a similar size to trypanosomes (Figure
10E).
257
Morphology:- A
• Leishmania tropica amastigotes from a
skin touch preparation
• In A, a still intact macrophage is practically
filled with amastigotes, several of which B
have clearly visible a nucleus and a
kinetoplast (arrows);
• In B, amastigotes are being freed from a
rupturing macrophage.
• Patient with history of travel to Egypt,
C
Africa, and the Middle East.
• Culture in NNN medium followed by
isoenzyme analysis identified the species
as L. tropica minor D
• The amastigotes are lining the wall of two
vacuoles, a typical arrangement (D)
258
Morphology:-
• Leishmania donovani, leptomonad E
forms (E)
• Bone marrow smear showing
Leishmania donovani parasites in a F
bone marrow histiocyte from a dog
(Giemsa stain) (F)
• Leishmania donovani in bone marrow
cell. Smear (G) G
• Giemsa stained leishmanial
promastigotes from a culture in which
the bar-shaped kinetoplast in the H
organism closest to the center of the
group "rosette" may be
seen
259
LEISHMANIASIS
Life cycle
• The organism is transmitted by the bite of several
species of blood-feeding sand flies (Phlebotomus) which
carry the promastigote in the anterior gut and pharynx
• The parasites gain access to mononuclear phagocytes
where they transform into amastigotes and divide until
the infected cell ruptures. The released organisms infect
other cells
• The sandfly acquires the organisms during the blood
meal; the amastigotes transform into flagellate
promastigotes and multiply in the gut until the anterior
gut and pharynx are packed. Dogs and rodents are
common reservoirs
260
261
LIFE CYCLE
• Leishmaniasis is transmitted by the bite of female
phlebotomine sandflies.
• The sandflies inject the infective stage, promastigotes, during
blood meals
• Promastigotes that reach the puncture wound are
phagocytized by macrophages and transform into
amastigotes
• Amastigotes multiply in infected cells and affect different
tissues, depending in part on the Leishmania species
• This originates the clinical manifestations of leishmaniasis.
• Sandflies become infected during blood meals on an infected
host when they ingest macrophages infected with amastigotes
• In the sandfly's midgut, the parasites differentiate into
promastigotes , which multiply and migrate to the proboscis
262
SYMPTOMS
Visceral leishmaniasis (kala-azar, dumdum fever):
• L. donovani organisms in visceral leishmaniasis are rapidly
eliminated from the site of infection, hence there is rarely a local
lesion, although minute papules have been described in children.
• They are localized and multiply in the mononuclear phagocytic
cells of spleen, liver, lymph nodes, bone marrow, intestinal
mucosa and other organs.
• One to four months after infection, there is occurrence of fever,
with a daily rise to 102-104 degrees F, accompanied by chills and
sweating.
• The spleen and liver progressively become enlarged. With
progression of the diseases, skin develops hyperpigmented
granulomatous areas (kala-azar means black disease).
• Chronic disease renders patients susceptible to other infections.
Untreated disease results in death.
263
Visceral leishmaniasis B
• Profile view of a teenage boy
suffering from visceral leishmaniasis.
The boy exhibits splenomegaly,
distended abdomen and severe
muscle wasting (B) C
• A 12-year-old boy suffering from
visceral leishmaniasis. The boy
exhibits splenomegaly and severe
muscle wasting (C)
E
• Enlarged spleen and liver in an
autopsy of an infant dying of visceral
leishmaniasis (E).
264
SYMPTOMS
Cutaneous leishmaniasis (Oriental sore, Delhi ulcer,
Baghdad boil):
• In cutaneous leishmaniasis, the organism (L. tropica)
multiplies locally, producing of a papule, 1-2 weeks (or
as long as 1-2 months) after the bite.
• The papule gradually grows to form a relatively painless
ulcer.
• The center of the ulcer encrusts while satellite papules
develop at the periphery.
• The ulcer heals in 2-10 months, even if untreated but
leaves a disfiguring scar (figure 12).
• The disease may disseminate in the case of depressed
immune function.
265
Cutaneous leishmaniasis A
• Skin ulcer due to leishmaniasis, hand of
Central American adult (A)
• Crater lesion of leishmaniasis (B)
• Scar on skin of upper leg representing
B
healed lesion of leishmaniasis (C)
• Non-healing cutaneous leishmaniasis
lesion on ear lobe (D) C
• Cutaneous leishmaniasis skin lesion.
The lesion measured about 1 inch in
diameter and was moist with raised
borders. There was no drainage; D
however, the lesion did appear to be
infected (F)
F
266
SYMPTOMS
Mucocutaneous leishmaniasis (espundia, Uta,
chiclero):
• The initial symptoms of mucocutaneous
leishmaniasis are the same as those of cutaneous
leishmaniasis, except that in this disease the
organism can metastasize and the lesions spread
to mucoid (oral, pharyngeal and nasal) tissues
and lead to their destruction and hence sever
deformity
• The organisms responsible are L. braziliensis, L.
mexicana and L. peruviana.
267
Mucocutaneous leishmaniasis
• Girl with diffuse muco-
cutaneous leishmaniasis E
of the face which is
responding to
treatment (E)
268
269
PATHOLOGY
• Pathogenesis of leishmaniasis is due to an
immune reaction to the organism, particularly cell
mediated immunity.
• Laboratory examination reveals a marked
leukopenia with relative monocytosis and
lymphocytosis, anemia and thrombocytopenia.
• IgM and IgG levels are extremely elevated due to
both specific antibodies and polyclonal activation.
270
DIAGNOSIS
• Diagnosis is based on a history of exposure to
sandfies, symptoms and isolation of the
organisms from the lesion aspirate or biopsy, by
direct examination or culture.
• A skin test (delayed hypersensitivity: Montenegro
test) and detection of anti-leishmanial antibodies
by immuno-fluorescence are indicative of
exposure.
271
• Sodium stibogluconate (Pentostam) is the
drug of choice.
• Pentamidine isethionate is used as an
alternative.
• Control measures involve vector control and
avoidance.
• Immunization has not been effective.
272
MALARIA
Etiology
• Four Plasmodium species are responsible for
human malaria
• These are
– P. falciparum,
– P. vivax,
– P. ovale and
– P. malariae.
273
MALARIA
Epidemiology
• There are an estimated 200 million global cases of
malaria leading a mortality of more than one million
people per year.
• P. falciparum (malignant tertian malaria) and P.
malariae (quartan malaria) are the most common
species of malarial parasite and are found in Asia and
Africa.
• P. vivax (benign tertian malaria) predominates in Latin
America, India and Pakistan,
• Whereas, P. ovale (ovale tertian malaria) is almost
exclusively found in Africa (figure 12G).
274
MALARIA:Epidemiology
• Malaria generally occurs in
areas where environmental
conditions allow parasite
multiplication in the vector.
• Thus, malaria is usually
restricted to tropical and
subtropical areas (see map)
and altitudes below 1,500 m.
• However, this distribution
might be affected by climatic
changes, especially global
warming, and population
movements.
275
MALARIA:Epidemiology
• Both Plasmodium falciparum and P.
malariae are encountered in all
shaded areas of the map (with P.
falciparum by far the most
prevalent).
• Plasmodium vivax and P. ovale are
traditionally thought to occupy
complementary niches, with P.
ovale predominating in Sub-Saharan
Africa and P. vivax in the other
areas;
• However these two species are not
always distinguishable on the basis
of morphologic characteristics
alone; the use of molecular tools
will help clarify their exact
distribution.
276
MALARIA:Morphology
• Malarial parasite trophozoites are generally
ring shaped, 1-2 microns in size, although
other forms (ameboid and band) may also
exist.
• The sexual forms of the parasite
(gametocytes) are much larger and 7-14
microns in size.
• P. falciparum is the largest and is banana
shaped while others are smaller and round. P.
vivax causes stippling of infected red cells
(figure 13-17). 277
Morphology:
P. falciparum
• Blood Stage Parasites (Thin
Blood Smears)
• Fig. 1: Normal red cell;
• Figs. 2-18: Trophozoites
(among these, Figs. 2-10
correspond to ring-stage
trophozoites);
• Figs. 19-26: Schizonts (Fig. 26
is a ruptured schizont);
• Figs. 27, 28: Mature
macrogametocytes (female);
microgametocytes (male)
278
Morphology: P. falciparum
• Blood Stage Parasites:

Thick Blood Smears
279
Morphology: P. falciparum
• Plasmodium falciparum:
Gametocytes
macrogametocytes (female);
• Fig. 29, 30: Mature
microgametocytes (male)
• Young gametocytes in the
peripheral blood
• Mature gametocytes
280
Morphology:
P. malariae
• Blood Stage Parasites:
Thin Blood Smears
• Fig. 1: Normal red cell; Figs. 2-5:
Young trophozoites (rings);
• Figs. 6-13: Trophozoites;
• Figs. 14-22: Schizonts; Fig. 23:
Developing gametocyte;
• Fig. 24: Macrogametocyte
(female);
• Fig. 25: Microgametocyte
(male)
281
Morphology: P. malariae
• Blood Stage
Parasites: Thick
Blood Smears
282
Morphology:
P. ovale
• Blood Stage Parasites: Thin
Blood Smears
• Figs. 2-5: Young
trophozoites (Rings);
• Figs. 16-23: Schizonts;
• Fig. 24: Macrogametocytes
(female);
(male)
283
Morphology:
P. vivax
• Blood Stage Parasites: Thin
Blood Smears
• Figs. 2-6: Young trophozoites
(ring stage parasites);
• Figs. 19-27: Schizonts;
• Figs. 28 and 29:
Macrogametocytes (female);
(male)
284
Malaria: Life cycle
• Malarial parasites are transmitted by the infected female
anopheline mosquito which injects sporozoites present in
the saliva of the insect (Figure 18).
• Sporozoites infect the liver parenchymal cells where they
may remain dormant (hypnozoites) or undergo stages of
schizogony to produce schizonts and merogony to produce
merozoites (meronts).
• When parenchymal cells rupture, thousands of meronts are
released into blood and infect the red cells.
• P. ovale and P. vivax infect immature red blood cells
whereas P. malariae infects mature red cells. P.
falciparum infects both.
• In red cells, the parasites mature into trophozoites. These
trophozoites undergo schizogony and merogony in red cells
which ultimately burst and release daughter merozoites.
285
Malaria: Life cycle
• Malarial parasites are transmitted by the infected female
anopheline mosquito which Some of the merozoites
transform into male and female gametocytes while others
enter red cells to continue the erythrocytic cycle.
• The gametocytes are ingested by the female mosquito, the
female gametocyte transforms into ookinete, is fertilized,
and forms an oocyst (figure 20) in the gut.
• The oocyte produces sporozoites (sporogony) which
migrate to the salivary gland and are ready to infect
another host.
• The liver (extraerythrocytic) cycle takes 5-15 days whereas
the erythrocytic cycle takes 48 hours or 72 hours (P.
malariae).
• Malaria can be transmitted by transfusion and
transplacentally. 286
287
Malaria: Life cycle
• The malaria parasite life cycle involves two hosts.
• During a blood meal, a malaria-infected female
Anopheles mosquito inoculates sporozoites into the
human host (1)
• Sporozoites infect liver cells (2) and mature into
schizonts (3), which rupture and release merozoites (4) .
• In P. vivax and P. ovale a dormant stage, hypnozoites
can persist in the liver and cause relapses by invading
the bloodstream weeks, or even years later.
288
Malaria: Life cycle
• After this initial replication in the liver (exo-erythrocytic
schizogony), the parasites undergo asexual
multiplication in the erythrocytes (erythrocytic
schizogony )
• Merozoites infect red blood cells (5). The ring stage
trophozoites mature into schizonts, which rupture
releasing merozoites (6)
• Some parasites differentiate into sexual erythrocytic
stages (gametocytes) (7)
• Blood stage parasites are responsible for the clinical
manifestations of the disease.
289
Malaria: Life cycle
• The gametocytes, male (microgametocytes) and female
(macrogametocytes), are ingested by
an Anophelesmosquito during a blood meal (8)
• The parasites’ multiplication in the mosquito is known
as the sporogonic cycle
• While in the mosquito's stomach, the microgametes
penetrate the macrogametes generating zygotes (9)
• The zygotes in turn become motile and elongated
(ookinetes) (10) which invade the midgut wall of the
mosquito where they develop into oocysts (11)
• The oocysts grow, rupture, and release sporozoites (12),
which make their way to the mosquito's salivary glands.
• Inoculation of the sporozoites into a new human host
perpetuates the malaria life cycle (1)
290
Malaria: Symptoms
• The symptomatology of malaria depends on the parasitemia,
the presence of the organism in different organs and the
parasite burden.
• The incubation period varies generally between 10-30 days.
• As the parasite load becomes significant, the patient
develops headache, lassitude, vague pains in the bones and
joints, chilly sensations and fever.
• As the disease progresses, the chills and fever become more
prominent.
• The chill and fever follow a cyclic pattern (paroxysm) with the
symptomatic period lasting 8-12 hours.
• In between the symptomatic periods, there is a period of
relative normalcy, the duration of which depends upon the
species of the infecting parasite.
• This interval is about 34-36 hours in the case of P.
vivax and P. ovale (tertian malaria), and 58-60 hours in the
case of P. malariae (quartan malaria). 291
Malaria: Symptoms
• Classical tertian paroxysm is rarely seen
in P. falciparum and persistent spiking or a daily
paroxysm is more usual.
• The malarial paroxysm is most dramatic and frightening.
• It begins with a chilly sensation that progresses to teeth
chattering, overtly shaking chill and peripheral
vasoconstriction resulting in cyanotic lips and nails (cold
stage).
• This lasts for about an hour. At the end of this period,
the body temperature begins to climb and reaches 103-
106 degrees F (39- 41degrees C).
• Fever is associated with severe headache, nausea
(vomiting) and convulsions.
• The patient experiences euphoria, and profuse
perspiration and the temperature begins to drop. 292
Malaria: Symptoms
• Within a few hours the patient feels exhausted but
symptom-less and remains symptomatic until the next
paroxysm.
• Each paroxysm is due to the rupture of infected
erythrocytes and release of parasites.
• Without treatment, all species of human malaria may
ultimately result in spontaneous cure except with P.
falciparum which becomes more severe progressively
and results in death.
• This organism causes sequestration of capillary
vasculature in the brain, gastrointestinal and renal
tissues
• Chronic malaria results in splenomegaly, hepatomegaly
and nephritic syndromes.
293
Malaria: Pathology and immunology
• Symptoms of malaria are due to the release of massive
number of merozoites into the circulation.
• Infection results in the production of antibodies which
are effective in containing the parasite load.
• These antibodies are against merozoites and schizonts.
• The infection also results in the activation of the
reticuloendothelial system (phagocytes).
• The activated macrophages help in the destruction of
infected (modified) erythrocytes and antibody-coated
merozoites.
• Cell mediated immunity also may develop and help in
the elimination of infected erythrocytes.
• Malarial infection is associated with
immunosuppression.
294
Malaria
Diagnosis
• Diagnosis is based on symptoms and detection of
parasite in Giemsa stained blood smears.
• There are also antibody tests
Treatment and Control

• Treatment is effective with various quinine derivatives
(quinine sulphate, chloroquine, meflaquine and
primaquine, etc.).
• Drug resistance, particularly in P. falciparum and to
some extent in P. vivax is a major problem.
• Control measures are eradication of infected anopheline
mosquitos.
• Vaccines are being developed and tried but none is
available yet for routine use. 295
BABESIOSIS
Etiology:-
• Babesia microti is the only member of the
genus that infects man.
Morphology:-
• The trophozoite is very similar to the ring form
of the Plasmodium species (figure A and B).
296
BABESIOSIS: Morphology
• Babesia microti infection, Giemsa- A
stained thin smear (A).
• The organisms resemble P. falciparum;
however Babesia parasites present
several distinguishing features: they B
vary more in shape and in size; and
they do not produce pigment
• Giemsa-stained thin smears. Note the
tetrad (left side of the image), a D
dividing form pathognomonic for
Babesia (B)
• Thin blood film of B. microti ring forms
with a typical Maltese Cross (four rings
in cross formation) (D)
297
BABESIOSIS : Life cycle
• The organism (sporozoite) is transmitted by a
tick and enters the red cell where it undergoes
mitosis and the organisms (merozoite) are
released to infect other red cells.
• Ticks acquire the organism during feeding on
an infected individual.
• In the tick, the organism divides sexually in the
gut and migrates into the salivary gland (figure
C).
298
299
• The Babesia microti life cycle involves two hosts, which
includes a rodent, primarily the white-footed
mouse, Peromyscus leucopus.
• During a blood meal, a Babesia-infected tick introduces
sporozoites into the mouse host (1)
• Sporozoites enter erythrocytes and undergo asexual
reproduction (budding) (2)
• In the blood, some parasites differentiate into male and
female gametes although these cannot be distinguished
at the light microscope level (3)
• The definitive host is a tick, in this case the deer
tick, Ixodes dammini (I. scapularis).
• Once ingested by an appropriate tick (4) , gametes unite
and undergo a sporogonic cycle resulting in sporozoites
(5)
300
• Transovarial transmission (also known as vertical, or
hereditary, transmission) has been documented for
“large” Babesia spp. but not for the “small”
babesiae, such as B. microti
• Humans enter the cycle when bitten by infected
ticks.
• During a blood meal, a Babesia-infected tick
introduces sporozoites into the human host (6)
• Sporozoites enter erythrocytes and undergo asexual
replication (budding) (7)
• Multiplication of the blood stage parasites is
responsible for the clinical manifestations of the
disease.
301
• Humans are, for all practical purposes, dead-end
hosts and there is probably little, if any, subsequent
transmission that occurs from ticks feeding on
infected persons.
• However, human to human transmission is well
recognized to occur through blood transfusions (8)
• Note: Deer are the hosts upon which the adult ticks
feed and are indirectly part of the Babesia cycle as
they influence the tick population.
• When deer populations increase, the tick population
also increases, thus heightening the potential for
transmission.
302
BABESIOSIS
Symptoms
• Babesiosis is associated with hemolytic anemia,
jaundice, fever and hepatomegaly, usually 1-2 weeks
after infection.
Diagnosis
• Diagnosis is based on symptoms, patient history and
detection of intraerythrocytic parasite in the patient or
transfer of blood in normal hamsters which can be
heavily parasitized.
• Drugs of choice are clindamycin combined with quinine.
The patient may recover spontaneously.
• One should avoid tick exposure and, if bitten, remove
the tick from the skin immediately.
303
TOXOPLASMOSIS
Etiology
• Toxoplasma gondii is the organism responsible
for toxoplasmosis
Epidemiology
• Toxoplasma has worldwide distribution and 20%-
75% of the population is seropositive without any
symptomatic episode.
• However, the infection poses a serious threat in
immunosuppressed individuals and pregnant
females
304
TOXOPLASMOSIS
Morphology
• The intracellular parasites (tachyzoite) are 3x6
microns, pear-shaped organisms that are
enclosed in a parasite membrane to form a cyst
measuring 10-100 microns in size.
• Cysts in cat feces (oocysts) are 10-13 microns in
diameter (figure).
305
TOXOPLASMOSIS: Morphology
• Toxoplasma gondii in the
bronchoalveolar lavage (BAL) material A
from an HIV infected patient (A).
• Numerous trophozoites (tachyzoites)
can be seen, which are typically
crescent shaped with a prominent,
centrally placed nucleus.
• Most of the tachyzoites are free, some
are still associated with B
bronchopulmonary cells.
• Toxoplasma gondii in tissue form of a
cat (B)
306
TOXOPLASMOSIS: Life cycle
• The natural life cycle of T. gondii occurs in cats and small
rodents, although the parasite can grow in the organs
(brain, eye, skeletal muscle, etc.) of any mammal or
birds (Figure 22).
• Cats gets infected by ingestion of cysts in flesh.
• Decystation occurs in the small intestine, and the
organisms penetrate the submucosal epithelial cells
where they undergo several generations of mitosis,
finally resulting in the development of micro- (male) and
macro- (female) gametocytes.
• Fertilized macro-gametocytes develop into oocysts that
are discharged into the gut lumen and excreted.
• Oocysts sporulate in the warm environment and are
infectious to a variety of animals including rodents and
man.
307
Life cycle
308
• Sporozoites released from the oocyst in the small
intestine penetrate the intestinal mucosa and find their
way into macrophages where they divide very rapidly
(hence the name tachyzoites) (figure 23) and form a cyst
which may occupy the whole cell.
• The infected cells ultimately burst and release the
tachyzoites to enter other cells, including muscle and
nerve cells, where they are protected from the host
immune system and multiply slowly (bradyzoites).
• These cysts are infectious to carnivores (including man).
Unless man is eaten by a cat, it is a dead-end host.
309
• Members of the cat family (Felidae) are the only known
definitive hosts for the sexual stages of T. gondii and thus are
the main reservoirs of infection.
• Cats become infected with T. gondii by carnivorism. After
tissue cysts or oocysts are ingested by the cat, viable organisms
are released and invade epithelial cells of the small intestine
where they undergo an asexual followed by a sexual cycle and
then form oocysts, which are then excreted.
• The unsporulated oocyst takes 1 to 5 days after excretion to
sporulate (become infective).
• Although cats shed oocysts for only 1 to 2 weeks, large
numbers may be shed.
• Oocysts can survive in the environment for several months and
are remarkably resistant to disinfectants, freezing, and drying,
but are killed by heating to 70°C for 10 minutes.
310
• Human infection may be acquired in several
ways:-
– A) ingestion of undercooked infected meat
containing Toxoplasma cysts;
– B) ingestion of the oocyst from fecally contaminated
hands or food;
– C) organ transplantation or blood transfusion;
– D) transplacental transmission;
– E) accidental inoculation of tachyzoites.
• The parasites form tissue cysts, most commonly
in skeletal muscle, myocardium, and brain; these
cysts may remain throughout the life of the host.
311
TOXOPLASMOSIS: Symptoms
• Although Toxoplasma infection is common, it
rarely produces symptoms in normal individuals.
• Its serious consequences are limited to pregnant
women and immunodeficient hosts.
• Congenital infections occur in about 1-5 per 1000
pregnancies of which 5-10% result in miscarriage
and 8-10% result in serious brain and eye
damage to the fetus. 10-13% of the babies will
have visual handicaps.
312
TOXOPLASMOSIS: Symptoms
• Although 58-70% of infected women will give
birth to a normal offspring, a small proportion of
babies will develop active retino-chorditis or
mental retardation in childhood or young
adulthood.
• In immunocompetent adults, toxoplasmosis, may
produce flue-like symptoms, sometimes
associated with lymphadenopathy.
• In immunocompromised individuals, infection
results in generalized parasitemia involvement of
brain, liver lung and other organs, and often
death.
313
TOXOPLASMOSIS
Immunology
• Both humoral and cell mediated immune responses are
stimulated in normal individuals. Cell-mediated
immunity is protective and humoral response is of
diagnostic value.
Diagnosis
• Suspected toxoplasmosis can be confirmed by isolation
of the organism from tonsil or lymph gland biopsy.
Treatment
• Acute infections benefit from pyrimethamine or
sulphadiazine. Spiramycin is a successful alternative.
Pregnant women are advised to avoid cat litter and to
handle uncooked and undercooked meat carefully.
314
PNEUMOCYSTIS PNEUMONIA
• Pneumocystis jiroveci (formerly known as
Pneumocystis carinii)
• Pneumocystis jiroveci was formerly thought to be
a protozoan but is now known to be a fungus.
• It is included here because pneumocystis
pneumonia is often described as an opportunistic
parasitic disease.
• Pneumocystis pneumonia is an infection of
immunosuppressed individuals and is particularly
seen in AIDS patients.
315
PNEUMOCYSTIS PNEUMONIA
• The organism is pleomorphic, exhibiting, at various
stages of its life cycle: 1-2 micron sporozoites, 4-5 micron
trophozoites and 6-8 micron cysts.
• It spreads from person to person in cough droplets.
Infection in immunosuppressed individuals results in
interstitial pneumonia characterized by thickened
alveolar septum infiltrated with lymphocytes and plasma
cells.
• Pneumonia is associated with fever, tachypnea, hypoxia,
cyanosis and asphyxia.
• Diagnosis is based on isolation of organisms from
affected lungs.
• Trimethoprim-sulphamethoxazole is the treatment of
choice 316
Morphology A
• Pneumocystis jiroveci trophozoites in
broncho-alveolar lavage (BAL) material (A).
Giemsa stain. The trophozoite are small (size:
1-5 µm), and only their nuclei, stained
purple, are visible (arrows)
• Pneumocystis jiroveci cysts (B). 3 cysts in
bronchoalveolar material;
• The rounded cysts (size 4-7 µm) contain 6-8
intracystic bodies, whose nuclei are stained B
by Giemsa;
• Note the presence of several smaller,
isolated trophozoites.
• Cysts in lung tissue, silver stain; the walls of
the cysts are stained black; the intracystic
bodies are not visible with this stain; baby C
who died with pneumonia (C) 317
Generalized life cycle of Pneumocystis
• These fungi are found in the lungs of mammals where they reside
without causing overt infection until the host's immune system
becomes debilitated.
• Then, an often times lethal pneumonia can result. Asexual phase:
trophic forms (1) replicate by mitosis (2) to (3) Sexual phase:
haploid trophic forms conjugate (1) and produce a zygote or
sporocyte (early cyst) (2) .
• The zygote undergoes meiosis and subsequent mitosis to produce
eight haploid nuclei (late phase cyst) (3)
• Spores exhibit different shapes (such as, spherical and elongated
forms). It is postulated that elongation of the spores precedes
release from the spore case.
• It is believed that the release occurs through a rent in the cell
wall. After release, the empty spore case usually collapses, but
retains some residual cytoplasm (4) .
• A trophic stage, where the organisms probably multiply by binary
fission is also recognized to exist. The organism causes disease in
immunosuppressed individuals. 318
life cycle of Pneumocystis 319
FACULTATIVE PARASITIC PROTOZOA
• These are free-living amebae that occasionally

cause serious human disease.
• They are of particular significance in
immunocompromised hosts.
• Free-living amebae belonging to the
genera Acanthamoeba, Balamuthia,
and Naegleria are important causes of disease
in humans and animals.
320
Negleria fowleri:-
• This organism is a flagellate that may inhabit
warm waters (spas, warm springs, heated
swimming pools, etc.) and gain access via the
nasal passage to the brain and cause
encephalitis
321
Negleria fowleri:-
A
• Naegleria fowleri trophozoites,
cultured from cerebrospinal fluid.
These cells have characteristically
large nuclei, with a large, dark
staining karyosome (A).
• The amebae are very active and
extend and retract pseudopods B
(A)
• Naegleria fowleri trophozoite in
spinal fluid (B). Note the typically
large karyosome and the
monopodial locomotion (B). 322
Negleria fowleri:-
C
• Histopathology of
amebic
meningoencephalitis
due to Naegleria
fowleri. Direct
fluorescent antibody D
stain (C).
Naegleria infection of
brain (D)
323
Life Cycle
• Naegleria fowleri produces an acute, and usually lethal, central
nervous system (CNS) disease called primary amebic
meingoencephalitis (PAM).
• N. fowleri has three stages, cysts (1) , trophozoites (2) , and
flagellated forms (3) , in its life cycle.
• The trophozoites replicate by promitosis (nuclear membrane
remains intact) (4)
• Naegleria fowleri is found in fresh water, soil, thermal discharges
of power plants, heated swimming pools, hydrotherapy and
medicinal pools, aquariums, and sewage.
• Trophozoites can turn into temporary flagellated forms which
usually revert back to the trophozoite stage.
• Trophozoites infect humans or animals by entering the olfactory
neuroepithelium and reaching the brain.
• N. fowleri trophozoites are found in cerebrospinal fluid (CSF) and
tissue, while flagellated forms are found in CSF.
324
325
Acanthemeba
• Several species of free-living Acanthemeba are
pathogenic to man
• They normally reside in soil and can infect
children who swallow dirt while playing on the
ground.
• In normal individuals, the infection may cause
mild disease (pharyngitis) or remain
asymptomatic, but in immunodeficient
individuals, the organism may penetrate the
esophageal mucosa and reach the brain where it
causes granulomatous encephalitis
326
Acanthemeba A
• Acanthamoeba sp.
keratitis.
– A: Biopsy showing
a cyst;
– B: cyst, at a larger
magnification,
with a
characteristic B
shape, in corneal
scraping.
327
• Acanthamoeba spp. and Balamuthia
mandrillaris are opportunistic free-living
amebae capable of causing granulomatous
amebic encephalitis (GAE) in individuals with
compromised immune systems.
328
Acanthamoeba & Balamuthia
• Acanthamoeba spp. have been found in soil; fresh,
brackish, and sea water; sewage; swimming pools;
contact lens equipment; medicinal pools; dental
treatment units; dialysis machines; heating, ventilating,
and air conditioning systems; mammalian cell cultures;
vegetables; human nostrils and throats; and human and
animal brain, skin, and lung tissues.
• B. mandrillaris however, has not been isolated from the

environment but has been isolated from autopsy
specimens of infected humans and animals.
329
Acanthamoeba & Balamuthia
• Unlike N. fowleri, Acanthamoeba and Balamuthia have
only two stages, cysts and trophozoites , in their life
cycle.
• No flagellated stage exists as part of the life cycle. The
trophozoites replicate by mitosis (nuclear membrane
does not remain intact)
• The trophozoites are the infective forms and are believed
to gain entry into the body through the lower respiratory
tract, ulcerated or broken skin and invade the central
nervous system by hematogenous dissemination
• Acanthamoeba spp. and Balamuthia mandrillaris cysts
and trophozoites are found in tissue.
330
331
332
NEMATODES
Round Worms
333
NEMATODES (Round Worms)
TEACHING OBJECTIVES:
• Epidemiology, morbidity and mortality
• Morphology of the organisms
• Life cycle, hosts and vectors
• Disease, symptoms, pathogenesis and site
• Diagnosis
• Prevention and control
334
INTESTINAL NEMATODES
 Intestinal nematodes of importance to man are:
− Ascaris lumbricoides (roundworm),
− Trichinella spiralis (trichinosis),
− Trichuris trichiura (whipworm),
− Enterobius vermicularis (pinworm),
− Strongyloides stercoralis (Cochin-china
diarrhea),
− Ancylostoma duodenale and Necator americanes
(hookworms) and
− Dracunculus medinensis
335
INTESTINAL NEMATODES
 E. vermicularis and T. trichiura are exclusively

intestinal parasites.
 Other helminths listed above have both

intestinal and tissue phases
336
Ascaris lumbricoides
Large intestinal roundworm

337
Epidemiology:
• The annual global morbidity due to ascaris
infections is estimated at 1 billion with a
mortality of 20,000.
• Ascariasis can occur at all ages, but it is
more prevalent in the 5 to 9 years age
group.
• The incidence is higher in poor rural
populations.
338
Morphology:
• The average female worm measures 30 cm x
5mm. The male is smaller
339
Morphology:
• Ascaris lumbricoides adult male and female
340
Morphology:
• Ascaris lumbricoides larva in section of lung
341
• A fertilized Ascaris egg, still at the A
unicellular stage, as they are when
passed in stool (A)
• Eggs are normally at this stage B
when passed in the stool
• Complete development of the larva
requires 18 days under favourable
conditions
• Eggs, unfertilized (left) and fertilized C
(right) (B)
• Unfertilized egg. Prominent
mamillations of outer layer (C)
342
• Fertilized egg. The embryo can be A
distinguished inside the egg (A)
• Unfertilized egg with no outer
mamillated layer (decorticated) (B) B
• Two fertilized eggs from the same
patient, where embryos have begun to
develop (this happens when the stool
sample is not processed for several
days without refrigeration) (C) C
• The embryos in early stage of division
(4-6 cells) can be clearly seen. Note
that the egg on the top has a very thin C
mamillated outer layer (C)
343
• Egg containing a larva, which A

will be infective if ingested (A)
• Larva hatching from an egg (B)
344
Ascaris Life Cycle
• Adult worms live in the lumen of the small
intestine.
• A female may produce approximately 200,000
eggs per day, which are passed with the feces .
• Unfertilized eggs may be ingested but are not
infective.
• Fertile eggs embryonate and become infective
after 18 days to several weeks, depending on the
environmental conditions (optimum: moist,
warm, shaded soil).
345
Ascaris Life Cycle
• After infective eggs are swallowed, the larvae hatch,
invade the intestinal mucosa, and are carried via the
portal, then systemic circulation to the lungs.
• The larvae mature further in the lungs (10 to 14 days),
penetrate the alveolar walls, ascend the bronchial tree
to the throat, and are swallowed
• Upon reaching the small intestine, they develop into
adult worms
• 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
346
Ascariasis Life Cycle 347
Ascaris Life Cycle
• The infection occurs by ingestion of food contaminated
with infective eggs which hatch in the upper small
intestine.
• The larvae (250 x 15 micrometers) penetrate the
intestinal wall and enter the venules or lymphatics.
• The larvae pass through the liver, heart and lung to
reach alveoli in 1 to 7 days during which period they
grow to 1.5 cm.
• They migrate up the bronchi, ascend the trachea to the
glottis, and pass down the oesophagus to the small
intestine where they mature in 2 to 3 months.
348
Ascaris Life Cycle
• A female may live in the intestine for 12 to 18 months
and has a capacity of producing 25 million eggs at an
average daily output of 200,000 (figure 2).
• The eggs are excreted in feces, and under suitable
conditions (21 to 30 0C, moist, aerated environment)
infective larvae are formed within the egg.
• The eggs are resistant to chemical disinfectant and
survive for months in sewage, but are killed by heat (40
degrees C for 15 minutes).
• The infection is man to man.
• Auto infection can occur.
349
Symptoms
• Symptoms are related to the worm burden.
• Ten to twenty worms may go unnoticed except in a
routine stool examination.
• The commonest complaint is vague abdominal pain.
In more severe cases, the patient may experience
listlessness (lack of energy and interest), weight loss,
anorexia (persistent loss of appetite), distended
abdomen, intermittent loose stool and occasional
vomiting.
• During the pulmonary stage, there may be a brief
period of cough, wheezing, dyspnea (difficulty in
breathing) and sub-sternal discomfort.
• Most symptoms are due to the physical presence of
the worm.
350
Diagnosis
• Diagnosis is based on identification of eggs
(40 to 70 micrometers by 35 to 50
micrometers) in the stool
351
Treatment and Prevention
• Mebendazole, 200 mg, for adults and 100 mg
for children, for 3 days is effective.
• Good hygiene is the best preventive
measure.
352
Trichinella spiralis
Trichinosis
353
Trichinella spiralis (Trichinosis)
Epidemiology:
• Trichinosis is related to the quality of pork and
consumption of poorly cooked meat.
• Autopsy surveys indicate about 2 percent of
the population is infected.
• The mortality rate is low.
354
Morphology:
• The adult female measures 3.5 mm x 60
micrometers.
• The larvae in the tissue (100 micrometers x
5 micrometers) are coiled in a lemon-shaped
capsule.
355
Morphology:
• Encysted larvae of Trichinella in pressed muscle
tissue.
• The coiled larvae can be seen inside the cysts
356
Morphology:
• Larvae of Trichinella, freed from their cysts,
typically coiled; length: 0.8 to 1 mm.
• Trichinella spiralis larvae in muscle section and
muscle press
357
Life cycle:
• Infection occurs by ingestion of larvae, in poorly cooked
meat, which immediately invade intestinal mucosa and
sexually differentiate within 18 to 24 hours.
• The female, after fertilization, burrows deeply in the
small intestinal mucosa, whereas the male is dislodged
(intestinal stage).
• On about the 5th day eggs begin to hatch in the female
worm and young larvae are deposited in the mucosa
from where they reach the lymphatics, lymph nodes and
the blood stream (larval migration).
• Larval dispersion occurs 4 to 16 weeks after infection.
358
Life cycle:
• The larvae are deposited in muscle fibres and, in
striated muscle, they form a capsule which
calcifies to form a cyst.
• In non-striated tissue, such as heart and brain, the
larvae do not calcify; they die and disintegrate.
• The cyst may persist for several years. One female
worm produces approximately 1500 larvae.
• Man is the terminal host.
• The reservoir includes most carnivorous and
omnivorous animals (Figure 3 and 4).
359
Life cycle 360

Trichinella spiralis, Life cycle
• Trichinellosis is acquired by ingesting meat containing
cysts (encysted larvae) (1) of Trichinella.
• After exposure to gastric acid and pepsin, the larvae are
released (2) from the cysts and invade the small bowel
mucosa where they develop into adult worms (3)
(female 2.2 mm in length, males 1.2 mm; life span in the
small bowel: 4 weeks).
• After 1 week, the females release larvae (4) that migrate
to the striated muscles where they encysted (5).
• Trichinella pseudospiralis, however, does not encyst.
• Encystment is completed in 4 to 5 weeks and the
encysted larvae may remain viable for several years. 361
Trichinella spiralis, Life cycle
• Ingestion of the encysted larvae perpetuates the cycle.
• Rats and rodents are primarily responsible for
maintaining the endemicity of this infection.
• Carnivorous/omnivorous animals, such as pigs or bears,
feed on infected rodents or meat from other animals.
• Different animal hosts are implicated in the life cycle of
the different species of Trichinella.
• Humans are accidentally infected when eating
improperly processed meat of these carnivorous
animals (or eating food contaminated with such meat).
362
Trichinella spiralis
Symptoms:
• Trichinosis symptoms depend on the severity of
infection: mild infections may be asymptomatic.
• A larger bolus of infection produces symptoms
according to the severity and stage of infection
and organs involved (Table 1).
363
Trichinosis : Symptoms:
Table 1
Trichinosis symptomatology
Intestinal Circulation and Myocardium Brain and
mucosa muscle (10-21 days) meninges
(24-72 hrs) (10-21 days) (14-28 days)
•Nausea •Edema, •Chest pain, •Headache
(unsettling feeling in •peri-orbital •tachycardia, (supraorbital),
the stomach with
conjunctivitis •EKG changes, •vertigo,
urge to vomit)
•photo phobia, •edema of •tinnitus,
•Vomiting •fever, chill, •deafness,
extremities,
•diarrhea •sweating, muscle •vascular •mental apathy,
•abdominal pain, spasm thrombosis. •delirium,
pain (involuntary sudden •coma,
•Headache muscle contraction,
•loss of reflexes.
•eosinophilia. 364
Trichinosis : Pathology and Immunology
• Trichinella pathogenesis is due the presence of large
numbers of larvae in vital muscles and host reaction to
larval metabolites.
• The muscle fibers become enlarged edematous and
deformed.
• The paralyzed muscles are infiltrated with neutrophil,
eosinophils and lymphocytes.
• Splenomegaly is dependent on the degree of infection.
• The worm induces a strong IgE response which, in
association with eosinophils, contributes to parasite
death.
365
Trichinosis : Diagnosis
• Diagnosis is based on symptoms, recent history
of eating raw or undercooked meat and
• Laboratory findings (eosinophilia, increased

serum creatine phosphokinase and lactate
dehydrogenase and antibodies to T. spiralis).
366
Trichinosis : Treatment and Control
• Steroids are used for treatment of inflammatory

symptoms and
• Mebendazole is used to eliminate worms.
• Elimination of parasite infection in hogs and
adequate cooking of meat are the best ways of
avoiding infection.
367
Trichuris trichiura
whipworm 368
Trichuris trichiura
Epidemiology:
• Trichuriasis is a tropical disease of children (5 to
15 yrs).
• It is concentrated in families and groups with
poorer sanitary habits.
369
Trichuris trichiura
Morphology:
• The female organism is 50 mm long with a
slender anterior (100 micrometer diameter) and
a thicker (500 micrometers diameter) posterior
end.
• The male is smaller and has a coiled posterior
end.
• The Trichuris eggs are lemon or football shaped
and have terminal plugs at both ends.
370
Trichuris trichiura
Morphology:
• Egg of Trichuris trichuria as seen on wet mount.
• The diagnostic characteristics are: a typical barrel
shape two polar plugs, that are unstained size:
50-54 µm by 22-23 µm.
• The external layer of the shell of the egg is
yellow-brown (in contrast to the clear polar
plugs).
• The egg is unembryonated, as eggs are when
passed with the stool
371
Trichuris trichiura
Morphology:
372
Trichuris trichiura
Morphology:
• Trichuris trichiura adult male and female
373
Trichuris trichiura
Life cycle
• Infection occurs by ingestion of embryonated
eggs in soil.
• The larva escapes the shell in the upper small
intestine and penetrates the villus where it
remains for 3 to 10 days.
• Upon reaching adolescence, the larvae pass to
the cecum and embed in the mucosa.
• They reach the ovipositing age in 30 to 90 days
from infection, produce 3000 to 10,000 eggs per
day and may live as long as 5 to 6 years. 374
Trichuris trichiura
Life cycle
• Eggs passed in feces embryonate in moist soil
within 2 to 3 weeks (Figure 5 and 6).
• The eggs are less resistant to desiccation, heat
and cold than ascaris eggs.
• The embryo is killed under desiccation at 37 0C
within 15 minutes.
• Temperatures of 52 0C and -9 0C are lethal.
375
Trichuris trichiura: Life cycle
376
Trichuris trichiura
Life cycle
• The unembryonated eggs are passed with the
stool (1).
• In the soil, the eggs develop into a 2-cell stage
(2), an advanced cleavage stage (3), and then
they embryonate (4); eggs become infective in
15 to 30 days.
• After ingestion (soil-contaminated hands or
food), the eggs hatch in the small intestine, and
release larvae (5) that mature and establish
themselves as adults in the colon (6).
377
Trichuris trichiura
Life cycle
• The adult worms (approximately 4 cm in length)
live in the caecum and ascending colon.
• The females begin to oviposit 60 to 70 days after
infection.
• Female worms in the caecum shed between
3,000 and 20,000 eggs per day.
• The life span of the adults is about 1 year
378
Trichuris trichiura
Symptoms:
• Symptoms are determined largely by the worm
burden: less than 10 worms are asymptomatic.
• Heavier infections (e.g., massive infantile
trichuriasis) are characterized by chronic profuse
mucus and bloody diarrhea with abdominal pains
and edematous prolapsed rectum.
• The infection may result in malnutrition, weight
loss and anemia and sometimes death.
379
Trichuris trichiura
Diagnosis:
• Diagnosis is based on symptoms and the
presence of eggs in feces (50 to 55 x 20 to 25
micrometers).
Treatment and Control:
• Mebendazole, 200 mg, for adults and 100 mg for
children, for 3 days is effective.
• Accompanying infections must be treated
accordingly.
• Improved hygiene and sanitary eating habits are
most effective in control.
380
Enterobius vermicularis
pinworm
381
Enterobius vermicularis (pinworm)
Epidemiology:
• Enterobiasis is by far the commonest
helminthic infection
• The worldwide infection is about 210 million.
• It is an urban disease of children in crowded
environment (schools, day care centres, etc.).
• Adults may get it from their children. The
incidence in whites is much higher than in
blacks.
382
Morphology:
• The female worm measures 8 mm x 0.5mm;
• the male is smaller.
• Eggs (60 micrometers x 27 micrometers) are
ovoid but asymmetrically flat on one side
383
Morphology:
• Enterobius vermicularis
adult male and female
• Enterobius vermicularis
adults in section of appendix
384
Morphology:
• Three eggs of Enterobius vermicularis A
collected from the same patient
examined directly on bright field.
• The diagnostic characteristics are: size
50-60 µm by 20-32 µm; typical B
elongated shape, with one convex side
and one flattened side; colorless shell
(here seen as a halo around the egg).
• The egg in A contains an embryo, while
those in B and C contain more
differentiated larvae, which are typically
coiled
C
385
Life cycle:
• Infection occurs when embryonated eggs are ingested from the
environment, with food or by hand to mouth contact.
• The embryonic larvae hatch in the duodenum and reach
adolescence in jejunum and upper ilium.
• Adult worms descend into lower ilium, cecum and colon and live
there for 7 to 8 weeks.
• The gravid females, containing more than 10,000 eggs migrate, at
night, to the perianal region and deposit their eggs there.
• Eggs mature in an oxygenated, moist environment and are
infectious 3 to 4 hours later.
• Man-to-man and auto infection are common (Figure 7 and 8).
Man is the only host.
386
Life cycle
387
Life cycle:
• Eggs are deposited on perianal folds (1).
• Self-infection occurs by transferring infective eggs to the
mouth with hands that have scratched the perianal area
(2).
• Person-to-person transmission can also occur through
handling of contaminated clothes or bed linens.
• Enterobiasis may also be acquired through surfaces in
the environment that are contaminated with pinworm
eggs (e.g., curtains, carpeting).
• Some small number of eggs may become airborne and
inhaled. These would be swallowed and follow the
same development as ingested eggs.
388
Life cycle:
• The time interval from ingestion of infective eggs to
oviposition by the adult females is about one month.
The life span of the adults is about two months. Gravid
females migrate nocturnally outside the anus and
oviposit while crawling on the skin of the perianal area
(5).
• The larvae contained inside the eggs develop (the eggs
become infective) in 4 to 6 hours under optimal
conditions (1).
• Retroinfection, or the migration of newly hatched larvae
from the anal skin back into the rectum, may occur but
the frequency with which this happens is unknown.
389
Symptoms:
• Enterobiasis is relatively innocuous (harmless or mild or
safe) and rarely produces serious lesions.
• The most common symptom is perianal, perineal and
vaginal irritation caused by the female migration.
• The itching results in insomnia and restlessness.
• In some cases gastrointestinal symptoms (pain, nausea,
vomiting, etc.) may develop.
• The conscientious housewife's mental distress, guilt
complex, and desire to conceal the infection from her
friends and mother-in-law is perhaps the most
important trauma of this persistent, pruritic parasite.
390
Diagnosis:
• Diagnosis is made by finding the adult worm or eggs in
the perianal area, particularly at night. Scotch tape or a
pinworm paddle is used to obtain eggs.
• Two doses (10 mg/kg; maximum of 1g each) of Pyrental
Pamoate two weeks apart gives a very high cure rate.
• Mebendazole is an alternative.
• The whole family should be treated, to avoid
reinfection.
• Bedding and underclothing must be sanitized between
the two treatment doses.
• Personal cleanliness provides the most effective in
prevention.
391
Strongyloides stercoralis
(Threadworm)
392
Strongyloides stercoralis (Threadworm)
Epidemiology:
• Threadworm infection, also known as Cochin-
China diarrhea, estimated at 50 to 100 million
cases worldwide, is an infection of the tropical
and subtropical areas with poor sanitation.
393
Morphology:
• The size and shape of threadworm varies
depending on whether it is parasitic or free-
living.
• The parasitic female is larger (2.2 mm x 45
micrometers) than the free-living worm (1 mm x
60 micrometers) (figure 10).
• The eggs, when laid are 55 micrometers by 30
micrometers.
394
Morphology:
• Strongyloides stercoralis:The
esophageal structure is clearly visible
in this larva; it consists of a club-
shaped anterior portion; a post-
median constriction; and a posterior
bulbus
• Note the prominent genital
primordium in the mid-section of the
larva; note also the Entamoeba coli
cyst near the tail of the larva
• Strongyloides stercoralis rhabditiform
larva
395
Strongyloides stercoralis: Life cycle
• The infective larvae of S. stercoralis penetrate the
skin of man, enter the venous circulation and
pass through the right heart to lungs, where they
penetrate into the alveoli.
• From there, the adolescent parasites ascend to
the glottis, are swallowed, and reach the upper
part of the small intestine, where they develop
into adults.
• Ovipositing females develop in 28 days from
infection. The eggs in the intestinal mucosa,
hatch and develop into rhabditiform larvae in
man. 396
• Alternatively, they are passed in the feces,
develop into infective filariform larvae and enter
another host to complete the direct cycle.
• If no suitable host is found, the larvae mature
into free-living worm and lay eggs in the soil.
• The eggs hatch in the soil and produce
rhabditiform larvae which develope into infective
filariform larvae and enter a new host (indirect
cycle), or mature into adult worms to repeat the
free-living cycle.
397
• The Strongyloides life cycle is complex among
helminths with its alternation between free-living
and parasitic cycles, and its potential for
autoinfection and multiplication within the host.
Two types of cycles exist:
• Free-living cycle: The rhabditiform larvae passed in
the stool (1) (see "Parasitic cycle" below) can either
molt twice and become infective filariform larvae
(direct development) (6) or molt four times and
become free living adult males and females (2) that
mate and produce eggs (3) from which rhabditiform
larvae hatch (4).
398
399
• The latter in turn can either develop (5) into a
new generation of free-living adults (as
represented in (2)), or into infective filariform
larvae (6). The filariform larvae penetrate the
human host skin to initiate the parasitic cycle
(see below) (6).
400
• Parasitic cycle: Filariform larvae in contaminated soil
penetrate the human skin (6), and are transported to
the lungs where they penetrate the alveolar spaces;
they are carried through the bronchial tree to the
pharynx, are swallowed and then reach the small
intestine (7).
• In the small intestine they molt twice and become adult
female worms (8). The females live threaded in the
epithelium of the small intestine and by
parthenogenesis produce eggs (9), which yield
rhabditiform larvae.
• The rhabditiform larvae can either be passed in the
stool (1) (see "Free-living cycle" above), or can cause
autoinfection (10). 401
• In autoinfection, the rhabditiform larvae become
infective filariform larvae, which can penetrate either
the intestinal mucosa (internal autoinfection) or the skin
of the perianal area (external autoinfection); in either
case, the filariform larvae may follow the previously
described route, being carried successively to the lungs,
the bronchial tree, the pharynx, and the small intestine
where they mature into adults; or they may disseminate
widely in the body.
• To date, occurrence of autoinfection in humans with
helminthic infections is recognized only in Strongyloides
stercoralis and Capillaria philippinensis infections. In the
case of Strongyloides, autoinfection may explain the
possibility of persistent infections for many years in
persons who have not been in an endemic area and of
hyperinfections in immunodepressed individuals
402
Necator americanes and
Ancylostoma duodenale
(Hookworms)
403
Hookworms
Epidemiology:
• Hookworms parasitize more than 900 million people
worldwide and cause daily blood loss of 7 million liters.
• Ancylostomiasis is the most prevalent hookworm
infection and is second only to ascariasis in infections by
parasitic worms.
• N. americanes (new world hookworm) is most common
in the Americas, central and southern Africa, southern
Asia, Indonesia, Australia and Pacific Islands.
• A. duodenale (old world hookworm) is the dominant
species in the Mediterranean region and northern Asia.
404
Hookworms
Morphology:
• Adult female hookworms are about 11 mm x 50
micrometers. Males are smaller.
• The anterior end of N. americanes is armed with
a pair of curved cutting plates whereas
A. duodenale is equipped with one or more pairs
of teeth.
• Hookworm eggs are 60 micrometers x 35
micrometers.
405
Hookworms
Morphology:
• Hookworm eggs examined on wet
mount (eggs of Ancylostoma
duodenale and Necator americanus
cannot be distinguished
morphologically).
• Diagnostic characteristics:-
• Size 57-76 µm by 35-47 µm, oval or
ellipsoidal shape, thin shell.
• The embryo in B has begun cellular
division and is at an early (gastrula)
developmental stage 406
Hookworms
Morphology:
• Ancylostoma duodenale adult male and
female
• Necator americanus adult female,
anterior end
• Necator americanus adult female,
anterior and posterior ends
• Necator americanus adult male,
posterior end
• Hookworm filariform larvae
407
Hookworms: Life cycle
• The life cycle of hookworms is identical to that of
threadworms, except that hookworms are not
capable of a free-living or auto-infectious cycle.
• Furthermore, A. duodenale can infect also by oral

route
408
409
• Eggs are passed in the stool (1), and under
favorable conditions (moisture, warmth, shade),
larvae hatch in 1 to 2 days.
• The released rhabditiform larvae grow in the
feces and/or the soil (2), and after 5 to 10 days
(and two molts) they become become filariform
(third-stage) larvae that are infective (3).
• These infective larvae can survive 3 to 4 weeks in
favorable environmental conditions.
• On contact with the human host, the larvae
penetrate the skin and are carried through the
veins to the heart and then to the lungs. 410
• They penetrate into the pulmonary alveoli, ascend the
bronchial tree to the pharynx, and are swallowed (4).
• The larvae reach the small intestine, where they reside
and mature into adults. Adult worms live in the lumen
of the small intestine, where they attach to the
intestinal wall with resultant blood loss by the host (5).
• Most adult worms are eliminated in 1 to 2 years, but
longevity records can reach several years.
• Some A. duodenale larvae, following penetration of the
host skin, can become dormant (in the intestine or
muscle).
• In addition, infection by A. duodenale may probably also
occur by the oral and transmammary route.
• N. americanus, however, requires a transpulmonary
migration phase 411
Hookworms: Symptoms
• Symptoms of hookworm infection depend on the
site at which the worm is present (Table 2) and
the burden of worms.
• Light infection may not be noticed
412
Hookworms: Symptoms
Table 2. Clinical features of hookworm disease
Site Symptoms Pathogenesis
Dermal •Local erythema, •Cutaneous invasion and

macules, papules subcutaneous migration of
(ground itch) larva
Pulmonary •Bronchitis, pneumonitis •Migration of larvae
and, sometimes, through lung, bronchi, and
eosinophilia trachea
Gastro- •Anorexia, epigastric •Attachment of adult
intestinal pain and gastro- worms and injury to upper
intestinal hemorrhage intestinal mucosa
Hematologic •Iron deficiency, anemia, •Intestinal blood loss
hypoproteinemia,
edema, cardiac failure 413
Hookworms: Diagnosis
• Diagnosis is made by identification of hookworm
eggs in fresh or preserved feces.
• Species of hookworms cannot be distinguished
by egg morphology.
414
Hookworms: Treatment and Control
• Mebendazole, 200 mg, for adults and 100 mg for
children, for 3 days is effective.
• Sanitation is the chief method of control:
sanitary disposal of fecal material and avoidance
of contact with infected fecal material.
415
Dracunculus medinensis
(Guinea worm; fiery serpent of the Israelites)

416
Epidemiology:
• There have been dramatic efforts to eradicate
Dracunculus.
• CDC estimated that in 1986 there were 3.5 million cases
worldwide.
• However, at the end of 2007, there were fewer than
10,000 reported cases in five nations in Africa: Sudan,
Ghana, Nigeria, Niger, and Mali, and as of June 2008,
cases had been reduced by more than 50 percent
compared to the same period of 2007.
• Guinea worm disease is expected to be the next disease
after smallpox to be eradicated and presently there may
be as few as 1000 cases worldwide.
417
Morphology:
• The adult female worm
measures 50-120 cm by 1 mm
and the male is half that size. A
• The female guinea worm
induces a painful blister (A);
after rupture of the blister, the
worm emerges as a whitish
filament (B) in the center of a
painful ulcer which is often
B
secondarily infected.
418
Morphology:
• Dracunculus medinensis worm wound around
matchstick.
• This helminth is gradually withdrawn from the
body by winding the stick
C
419
Dracunculus medinensis: Life cycle
• The infection is caused by ingestion of water
contaminated with water fleas (Cyclops) infected with
larvae.
• The rhabtidiform larvae penetrate the human digestive
tract wall, lodge in the loose connective tissues and
mature into the adult form in 10 to 12 weeks.
• In about a year, the gravid female migrates to the
subcutaneous tissue of organs that normally come in
contact with water and discharges its larvae into the
water (figure 13A).
• The larvae are picked up by Cyclops, in which they
develop into infective form in 2 to 3 weeks.
420
421
• Humans become infected by drinking unfiltered
water containing copepods (small crustaceans)
which are infected with larvae of D. medinensis
(1)
• Following ingestion, the copepods die and release
the larvae, which penetrate the host stomach and
intestinal wall and enter the abdominal cavity and
retroperitoneal space (2) .
• After maturation into adults and copulation, the
male worms die and the females (length: 70 to
120 cm) migrate in the subcutaneous tissues
towards the skin surface (3) .
422
• Approximately one year after infection, the
female worm induces a blister on the skin,
generally on the distal lower extremity, which
ruptures.
• When this lesion comes into contact with water, a
contact that the patient seeks to relieve the local
discomfort, the female worm emerges and
releases larvae (4) .
• The larvae are ingested by a copepod (5) and after
two weeks (and two molts) have developed into
infective larvae (6) .
• Ingestion of the copepods closes the cycle (1)
423
Dracunculus medinensis: Symptoms
• If the worm does not reach the skin, it dies and
causes little reaction.
• In superficial tissue, it liberates a toxic substance
that produces a local inflammatory reaction in the
form of a sterile blister with serous exudation.
• The worm lies in a subcutaneous tunnel with its
posterior end beneath the blister, which contains
clear yellow fluid.
• The course of the tunnel is marked with
induration and edema.
• Contamination of the blister produces abscesses,
cellulitis, extensive ulceration and necrosis. 424
Dracunculus medinensis: Diagnosis
• Diagnosis is made from the local blister, worm or

larvae.
• The outline of the worm under the skin may be
revealed by reflected light.
425
Dracunculus medinensis: Treatment
• Treatment includes the extraction of the adult

guinea worm by rolling it a few centimeters per
day or preferably by multiple surgical incisions
under local anaesthesia.
• Metronidazole is effective in killing the worm.
• Protection of drinking water from being
contaminated with Cyclops and larvae are
effective preventive measures.
426
Toxocara canis and T. catti
(visceral larva migrans)
427
• These are roundworms of dogs and cats but they
can infect humans and cause damage of the
visceral organs.
• Eggs from feces of infected animals are
swallowed by man and hatch in the intestine.
• The larvae penetrate the mucosa, enter the
circulation and are carried to liver, lungs, eyes
and other organs where they cause
inflammatory necrosis.
428
• Symptoms are due to the inflammatory reaction
at the site of infection.
• The most serious consequence of infection may
be loss of sight if the worm localizes in the eye.
• Treatment includes Mebendazole to eliminate
the worm and prednisone for inflammatory
symptoms.
• Avoidance of infected dogs and cats is the best
prevention
429
• Eggs of Toxocara canis. These eggs are
passed in dog feces, especially puppies'
feces.
• Humans do not produce or excrete
eggs, and therefore eggs are not a
diagnostic finding in human toxocariasis
• The egg to the left is fertilized but not
yet embryonated, while the egg to the
right contains a well developed larva.
• The latter egg would be infective if
ingested by a human (frequently, a
child).
• Toxocara canis (Dog Roundworm) egg,
embryonated
430
Toxocara Life Cycle
• Toxocara canis accomplishes its life cycle in dogs,
with humans acquiring the infection as
accidental hosts.
• Following ingestion by dogs, the infective eggs
yield larvae that penetrate the gut wall and
migrate into various tissues, where they encyst if
the dog is older than 5 weeks.
• In younger dogs, the larvae migrate through the
lungs, bronchial tree, and esophagus; adult
worms develop and oviposit in the small
intestine. 431
Toxocara Life Cycle 432
Toxocara Life Cycle
• In the older dogs, the encysted stages are reactivated
during pregnancy, and infect by the transplacental and
transmammary routes the puppies, in whose small
intestine adult worms become established.
• Thus, infective eggs are excreted by lactating bitches
and puppies.
• Humans are paratenic hosts who become infected by
ingesting infective eggs in contaminated soil.
• After ingestion, the eggs yield larvae that penetrate the
intestinal wall and are carried by the circulation to a
wide variety of tissues (liver, heart, lungs, brain, muscle,
eyes).
• While the larvae do not undergo any further
development in these sites, they can cause severe local
reactions that are the basis of toxocariasis.
433
Ancylostoma braziliensis
(cutaneous larva migrans, creeping

eruption) 434
Ancylostoma braziliensis (cutaneous larva
migrans, creeping eruption)
• Creeping eruption is prevalent in many
tropical and subtropical countries.
• The organism is primarily a hookworm of dogs
and cats but the filariform larvae in animal
feces can infect man and cause skin eruptions.
• Since the larvae have a tendency to move
around, the eruption migrates in the skin
around the site of infection.
435
Ancylostoma braziliensis (cutaneous larva
migrans, creeping eruption)
• The symptoms last the duration of larval
persistence which ranges from 2 to 10 weeks.
• Light infection can be treated by freezing the
involved area.
• Heavier infections are treated with
Mebendazole.
• Infection can be avoided by keeping away
from water and soil contaminated with
infected feces
436
Ancylostoma braziliensis
• Ancylostoma brasiliense adult male
and female
• Hookworm eggs examined on wet
mount (eggs of Ancylostoma
duodenale and Necator americanus
cannot be distinguished
morphologically).
• Diagnostic characteristics:
– Size 57-76 µm by 35-47 µm
– Oval or ellipsoidal shape
– Thin shell
– The embryo in B has begun cellular
division and is at an early (gastrula)
developmental stage
437
Ancylostoma braziliensis: Life Cycle
• Eggs are passed in the stool (1) , and under favorable
conditions (moisture, warmth, shade), larvae hatch in 1
to 2 days.
• The released rhabditiform larvae grow in the feces
and/or the soil (2) , and after 5 to 10 days (and two
molts) they become become filariform (third-stage)
larvae that are infective (3) .
• These infective larvae can survive 3 to 4 weeks in
favorable environmental conditions.
• On contact with the human host, the larvae penetrate
the skin and are carried through the veins to the heart
and then to the lungs.
438
439
• They penetrate into the pulmonary alveoli,
ascend the bronchial tree to the pharynx, and
are swallowed (4) .
• The larvae reach the small intestine, where they
reside and mature into adults.
• Adult worms live in the lumen of the small
intestine, where they attach to the intestinal wall
with resultant blood loss by the host (5)
440
• Most adult worms are eliminated in 1 to 2 years,
but longevity records can reach several years.
• Some A. duodenale larvae, following penetration
of the host skin, can become dormant (in the
intestine or muscle).
• In addition, infection by A. duodenale may
probably also occur by the oral and
transmammary route. N. americanus, however,
requires a transpulmonary migration phase.
441
BLOOD AND TISSUE
HELMINTHS
The major blood and tissue parasites of man are
microfilaria.
These include
Wuchereria bancrofti and Brugia malayi,
Onchocerca volvulus, and Loa loa (eye worm).
442
Wuchereria bancrofti
and
Brugia malayi
Elephantiasis
443
Wuchereria bancrofti and
Brugia malayi
Epidemiology:
• W. bancrofti is strictly a human pathogen and is
distributed in tropical areas worldwide, whereas
B. malayi infects a number of wild and domestic
animals and is restricted to South-East Asia.
• Mosquitoes are vectors for both parasites.
444
Brugia malayi
Morphology:
• These two organisms are very similar in morphology and
in the diseases they cause.
• Adult female W. bancrofti found in lymph nodes and
lymphatic channels are 10 cm x 250 micrometers
whereas males are only half that size.
• Microfilaria found in blood are only 260 micrometers x
10 micrometers.
• Adult B. malayi are only half the size of W. bancrofti but
their microfilaria are only slightly smaller than
W. bancrofti.
445
Brugia malayi A
Morphology:
• Figure A and B: Microfilaria of
Wuchereria bancrofti (Thick
blood smears stained with
hematoxylin).
• The microfilaria is sheathed, its
body is gently curved, and the B
tail is tapered to a point.
• The nuclear column (the cells
that constitute the body of the
microfilaria) is loosely packed, Microfilaria of Wuchereria
the cells can be visualized bancrofti collected by filtration
individually and do not extend with a nucleopore membrane.
to the tip of the tail. Giemsa stain, which does not
• The sheath is slightly stained demonstrate the sheath of this
with hematoxylin sheathed species. The pores of
the membrane are visible 446
Wuchereria bancrofti &
Brugia malayi
A
Morphology:
• Wuchereria bancrofti
microfilaria in peripheral
blood, giemsa stain
• Wuchereria bancrofti B
adults in section of
lymph node
447
Wuchereria bancrofti &
Brugia malayi
Morphology:
A
• Figure A Microfilaria of Brugia malayi.
• Thick blood smear, hematoxylin stain.
Like Wuchereria bancrofti, this species
has a sheath (slightly stained in
hematoxylin).
• Differently from Wuchereria, the
microfilariae in this species are more
tightly coiled, and the nuclear column is
more tightly packed, preventing the
visualization of individual cells
• Detail from the microfilaria of Brugia
malayi showing the tapered tail, with a
subterminal and a terminal nuclei (seen
as swellings at the level of the arrows), B
separated by a gap without nuclei. This
is characteristic of B. malayi.
448
Wuchereria bancrofti & Brugia malayi
Life cycle:
• Filariform larvae enter the human body during a
mosquito bite and migrate to various tissues.
• There, they may take up to a year to mature and
produce microfilaria which migrate to lymphatics
and, at night, enter the blood circulation.
• Mosquitos are infected during a blood meal. The
microfilaria grow 4 to 5 fold in the mosquito in 10
to 14 days and become infective for man.
449
Wuchereria bancrofti : Life cycle
450
• Different species of the following genera of mosquitoes
are vectors of W. bancrofti filariasis depending on
geographical distribution.
• Among them are:
– Culex (C. annulirostris, C. bitaeniorhynchus, C.
quinquefasciatus, and C. pipiens);
– Anopheles (A. arabinensis, A. bancroftii, A. farauti, A.
funestus, A. gambiae, A. koliensis, A. melas, A. merus, A.
punctulatus and A. wellcomei);
– Aedes (A. aegypti, A. aquasalis, A. bellator, A. cooki, A.
darlingi, A. kochi, A. polynesiensis, A. pseudoscutellaris, A.
rotumae, A. scapularis, and A. vigilax);
– Mansonia (M. pseudotitillans, M. uniformis);
– Coquillettidia (C. juxtamansonia).
451
• During a blood meal, an infected mosquito introduces
third-stage filarial larvae onto the skin of the human
host, where they penetrate into the bite wound (1).
• They develop in adults that commonly reside in the
lymphatics (2).
• The female worms measure 80 to 100 mm in length
and 0.24 to 0.30 mm in diameter, while the males
measure about 40 mm by 0.1 mm.
• Adults produce microfilariae measuring 244 to 296 μm
by 7.5 to 10 μm, which are sheathed and have
nocturnal periodicity, except the South Pacific
microfilariae which have the absence of marked
periodicity.
452
• The microfilariae migrate into lymph and blood
channels moving actively through lymph and blood (3).
• A mosquito ingests the microfilariae during a blood meal
(4).
• After ingestion, the microfilariae lose their sheaths and
some of them work their way through the wall of the
proventriculus and cardiac portion of the mosquito's
midgut and reach the thoracic muscles (5).
• There the microfilariae develop into first-stage larvae (6)
and subsequently into third-stage infective larvae (7).
• The third-stage infective larvae migrate through the
hemocoel to the mosquito's proboscis (8) and can infect
another human when the mosquito takes a blood meal (1).
453
Brugia malayi : Life cycle 454
Brugia malayi : Life cycle
• The typical vector for Brugia malayi filariasis are
mosquito species from the genera Mansonia
and Aedes.
• During a blood meal, an infected mosquito
introduces third-stage filarial larvae onto the
skin of the human host, where they penetrate
into the bite wound (1) .
• They develop into adults that commonly reside
in the lymphatics (2).
• The adult worms resemble those of Wuchereria
bancrofti but are smaller. 455
• Female worms measure 43 to 55 mm in length
by 130 to 170 μm in width, and males measure
13 to 23 mm in length by 70 to 80 μm in width.
• Adults produce microfilariae, measuring 177 to
230 μm in length and 5 to 7 μm in width, which
are sheathed and have nocturnal periodicity.
• The microfilariae migrate into lymph and enter
the blood stream reaching the peripheral blood
(3).
456
• A mosquito ingests the microfilariae during a blood
meal (4). After ingestion, the microfilariae lose their
sheaths and work their way through the wall of the
proventriculus and cardiac portion of the midgut to
reach the thoracic muscles (5).
• There the microfilariae develop into first-stage larvae
(6) and subsequently into third-stage larvae (7) .
• The third-stage larvae migrate through the hemocoel
to the mosquito's proboscis (8) and can infect another
human when the mosquito takes a blood meal (1).
457
W. bancrofti & B. malayi
Symptoms:
• Symptoms include lymphadenitis and recurrent
high fever every 8 to 10 weeks, which lasts 3 to 7
days.
• There is progressive lymphadenitis due to an
inflammatory response to the parasite lodged in
the lymphatic channels and tissues.
• As the worm dies, the reaction continues and
produces a fibro-proliferative granuloma which
obstructs lymph channels and causes
lymphedema and elephantiasis (figures).
458
Symptoms:
• The stretched skin is susceptible to traumatic
injury and infections.
• Microfilaria cause eosinophilia and some
splenomegaly.
• Not all infections lead to elephantiasis.
• Prognosis (or diagnosis), in the absence of
elephantiasis, is good.
459
Symptoms: elephantiasis
large hydrocoele
leopard skin 460

Diagnosis:
• Diagnosis is based on history of mosquito bites in
endemic areas, clinical findings and presence of
microfilaria in blood samples collected at night.
Treatment and control:
• Diethylcarbamazine quickly kills the adults worms or
sterilizes the female.
• It is given 2 mg/kg orally for 14 days.
• Steroids help alleviate inflammatory symptoms.
• Cooler climate reduces the inflammatory reaction.
461
Onchocerca volvulus
(Onchocerciasis)
Blinding filariasis or
river blindness
462
Onchocerciasis
Epidemiology:
• Onchocerciasis is prevalent throughout eastern,
central and western Africa, where it is the major
cause of blindness.
• In the Americas, it is found in Guatemala,
Mexico, Colombia and Venezuela.
• The disease is confined to neighbourhoods of
low elevation with rapidly flowing small streams
where black flies breed.
• Man is the only host.
463
Onchocerciasis
Morphology:
• Adult female Onchocerca
measure 50 cm by 300
micrometers, male worms
are much smaller.
• Infective larvae of O.
volvulus are 500
micrometers by 25
micrometers (figures).
464
Onchocerciasis
Morphology:
Onchocerca volvulus
nodule
• Onchocerca
volvulus adults in
section of tumour
• Face of a blind
male patient in
the
onchocerciasis
areas
• An old man,
blinded by
onchocerciasis
465
Onchocerciasis
Life cycle:
• Infective larvae are injected into human skin by the
female black fly (Simulium damnosum) where they
develop into adult worms in 8 to 10 months.
• The adults usually occur as group of tightly coiled
worms (2 to 3 females and 1 to 2 males).
• The gravid female releases microfilarial larvae, which
are usually distributed in the skin.
• They are picked up by the black fly during a blood meal.
• The larvae migrate from the gut of the black fly to the
thoracic muscle where they develop into infective larvae
in 6 to 8 days.
• These larvae migrate to the head of the fly and then are
transmitted to a second host.
466
Onchocerca volvulus: Life cycle
467
Onchocerciasis
Life cycle:
• During a blood meal, an infected black fly (genus
Simulium) introduces third-stage filarial larvae onto the
skin of the human host, where they penetrate into the
bite wound (1).
• In subcutaneous tissues the larvae (2) develop into adult
filarial worm, which commonly reside in nodules in
subcutaneous connective tissues (3).
• Adults can live in the nodules for approximately 15
years.
• Some nodules may contain numerous male and female
worms.
468
Onchocerciasis
Life cycle:
• Females measure 33 to 50 cm in length and 270 to 400
μm in diameter, while males measure 19 to 42 mm by
130 to 210 μm.
• In the subcutaneous nodules, the female worms are
capable of producing microfilariae for approximately 9
years.
• The microfilariae, measuring 220 to 360 µm by 5 to 9
µm and unsheathed, have a life span that may reach 2
years.
• They are occasionally found in peripheral blood, urine,
and sputum but are typically found in the skin and in the
lymphatics of connective tissues (4).
469
Onchocerciasis
Life cycle:
• A black fly ingests the microfilariae during a
blood meal (5).
• After ingestion, the microfilariae migrate from
the black fly's midgut through the hemocoel to
the thoracic muscles (6).
• There the microfilariae develop into first-stage
larvae (7) and subsequently into third-stage
infective larvae (8).
• The third-stage infective larvae migrate to the
black fly's proboscis (9) and can infect another
human when the fly takes a blood meal (1).
470
Onchocerciasis
Symptoms:
• Onchocerciasis results in nodular and erythematous
lesions in the skin and subcutaneous tissue due to a
chronic inflammatory response to persistent worm
infection.
• During the incubation period of 10 to 12 months, there
is eosinophilia and urticaria (skin rash).
• Ocular involvement consists of trapping of microfilaria
in the cornea, choroid, iris and anterior chambers,
leading to photophobia, lacrimation (production of
tears) and blindness (figures in prior slides).
471
Onchocerciasis
Diagnosis:
• Diagnosis is based on symptoms, history of exposure
to black flies and presence of microfilaria in nodules.
Treatment and control:

• Diethylcarbamazine is effective in killing the worm.
• Destruction of microfilaria produces extreme allergic
reaction which can be controlled with corticosteroids.
• Prevention measures include vector control, treatment
of infected individuals and avoidance of black fly.
472
Loa loa
(Loasis)
eye worm
473
Loa loa: Loasis
• Loasis is limited to the areas of African equatorial
rain forest.
• The incidence in endemic areas varies greatly (8
to 75 percent).
• The larger, female organisms are 60 mm by 500
micrometers; males are 35mm by 300
micrometers in size (figure 22).
• The circulating microfilaria are 300 micrometers
by 7 micrometers; the infective larvae in the fly
are 200 micrometers by 30 micrometers.
474
Loa loa, agent of filariasis
Morphology:
• Microfilariae of Loa loa (right) and
Mansonella perstans (left) (A). A
• Thick blood smear stained with
hematoxylin. Loa loa is sheathed,
with a relatively dense nuclear
B
column; its tail tapers and is
frequently coiled, and nuclei extend
to the end of the tail.
• Mansonella perstans is smaller, has
no sheath, and has a blunt tail with
nuclei extending to the end of the
tail.
• Loa loa, anterior end (B)
• Loa loa, posterior end (C) C 475
Loa loa: Loasis
• The life cycle of Loa loa (figure in next slide) is identical
to that of onchocerca except that the vector for this
worm is the deer fly.
• The infection results in subcutaneous (Calabar) swelling,
measuring 5 to 10 cm in diameter, marked by erythema
and angioedema, usually in the extremities.
• The organism migrates under the skin at a rate of up to
an inch every two minutes.
• Consequently, the swelling appears spontaneously,
persists for 4 to 7 days and disappears, and is known as
fugitive or Calabar swelling.
476
Loa loa: Loasis
• The worm usually causes no serious problems,
except when passing through the orbital
conjunctiva or the nose bridge.
• The diagnosis is based on symptoms, history of
deer fly bite and presence of eosinophilia.
• Recovery of worms from the conjunctiva is
confirmatory.
• Treatment and control are the same as those for
onchocerciasis.
477
Loa loa: Life Cycle 478
479
480
481
CESTODES (TAPE WORMS)
TEACHING OBJECTIVES
• Epidemiology, morbidity and mortality
• Morphology of the organism
• Life cycle, hosts and vectors
• Disease, symptoms, pathogenesis and site
• Diagnosis
• Prevention and control
482
CESTODES
(TAPE WORMS)
483
Introduction:-
• Clinically important cestodes pathogenic to
man are
– Tenia solium (pork tapeworm),
– T. saginata (beef tapeworm),
– Diphyllobothrium lattum (fish or broad
tapeworm),
– Hymenolepis nana (dwarf tapeworm) and
– Echinococcus granulosus and E. multilocularis
(hydatid).
484
General Features:-
• The subclass Cestoda of Phylum Platyhelminthes
contains the Tapeworms
• These worm have no digestive tract or mouth, and
attachment organs are limitted to the anterior end
• Because of the lack of mouth and digestive tract,
tapeworms have been called the most parasitic of all
parasites; that means they are highly specialized
• Cestodes or tapeworms are all parasitic in digestive
tracts and associated ducts of all classes of
vertebrates and some firsh water oligochaetes
485
General Morphology:-
• The anterior end of Tapeworms is called the
Scolex or Holdfast; it has various structures
for attachment including sucking depressions,
hooks, and glandular areas
• The sucking depressions are of three types:
bothria, a pair of shallow sucking grooves
typical of the Pseudophyllidea; bothridia,
four leaflike, flexible structures seen in the
orders including the important Cyclophyllidea
486
• A few tapeworms lack anterior holdfast structures,
but most have one of the three types mentioned
above
• In addition, some tapeworms have an apical organ,
the rostellum, which may have an additional sucker,
glandular area, or hooks (those scolices with hooks
are spoken of as being armed)
• Posterior to the scolex region there are two body
types:
• The first is a body of a single segment (monozoic)
and the other is a body of many segment (polyzoic)487
• Each segment is called a proglottid, and the chain of
proglottids is called a strobila
• Usually each proglottid has its own set of
reproductive organs.
• Tapeworms have the immature proglottids closest to
the scolex, then a region of sexually mature
proglottids, and finally gravid proglottids that have
uteri filled with eggs.
• Since tapeworms lack both a mouth and digestive
tract, all nutrients must be acquired through external
surface 488
1. Tenia solium & T. saginata (Teniasis)
Epidemiology:
• These cestodes have a worldwide distribution
but incidence is higher in developing
countries.
• Infection rate is as low as 1 per 1000 in most
of North America and as high as 10% in the
third world.
• Pork tapeworm shows a higher incidence but
this is dependent on dietary habits.
489
Morphology:-
• T. saginata can be up to 4 to 6 meters long and 12
mm broad; it has a pear-shaped head (scolex) with
four suckers but no hooks or neck.
• It has a long flat body with several hundred
segments (proglottids).
• Each segment is about 18 x 6 mm with a branched
uterus (15-30 branches).
• The egg is 35 x 45 micrometers, roundish and yellow-
brown. It has peripheral radial striations and
contains an embryo with 3 hooklets (figure2).
490
Morphology:-
• T. solium is slightly smaller than T. saginata. It
has a globular scolex with four suckers and a
circular row of hooks (rostellum) that gives it a
solar appearance.
• There is a neck and it has a long flat body (0.1
meter in length).
• The proglottids are 5 x 10 mm with a 7-12
branch uterus. The eggs of T. solium and T.
saginata are indistinguishable (figure2).
491
1. Tenia solium & T. saginata: Morphology
492
493
494
Life cycle of Taenia saginata and Taenia solium: -
• A tapeworm larval cyst (cysticercus) is ingested with
poorly cooked infected meat; the larva escapes the cyst
and passes to the small intestine where it attaches to
the mucosa by the scolex suckers.
• The proglottids develop as the worm matures in 3 to 4
months.
• The adult may live in the small intestine as long as 25
years and pass gravid proglottids with the feces.
• Eggs extruded from the proglottid contaminate and
persist on vegetation for several days and are consumed
by cattle or pigs in which they hatch and form cysticerci
(Figure below).
495
1. Tenia solium & T. saginata: Life cycle
496
1. Tenia solium & T. saginata: Life Cycle
• Humans are the only definitive hosts for Taenia saginata
and Taenia solium.
• Eggs or gravid proglottids are passed with feces (1) ; the
eggs can survive for days to months in the
environment.
• Cattle (T. saginata) and pigs (T. solium) become infected
by ingesting vegetation contaminated with eggs or
gravid proglottids (2).
• In the animal's intestine, the oncospheres hatch (3),
invade the intestinal wall, and migrate to the striated
muscles, where they develop into cysticerci.
497
• A cysticercus can survive for several years in the
animal. Humans become infected by ingesting raw or
undercooked infected meat (4).
• In the human intestine, the cysticercus develops over 2
months into an adult tapeworm, which can survive for
years.
• The adult tapeworms attach to the small intestine by
their scolex (5) and reside in the small intestine (6).
• Length of adult worms is usually 5 m or less for T.
saginata (however it may reach up to 25 m) and 2 to 7
m for T. solium.
498
• The adults produce proglottids which mature, become
gravid, detach from the tapeworm, and migrate to the
anus or are passed in the stool (approximately 6 per
day).
• T. saginata adults usually have 1,000 to 2,000
proglottids, while T. solium adults have an average of
1,000 proglottids.
• The eggs contained in the gravid proglottids are
released after the proglottids are passed with the feces.
T. saginata may produce up to 100,000 and T. solium
may produce 50,000 eggs per proglottid respectively.
499
1. Tenia solium & T. saginata: Symptoms
• Light infections remain asymptomatic, but heavier
infections may produce abdominal discomfort,
epigastric pain, vomiting and diarrhea.
Cysticercosis:-
• T. solium eggs can also infect humans and cause
cysticercosis (larval cysts in lung, liver, eye and brain)
resulting in blindness and neurological disorders.
• The incidence of cerebral cysticercosis can be as high 1
per 1000 population and may account for up to 20% of
neurological case in some countries (e.g., Mexico);
• Cysticercosis ocular involvement occurs in about 2.5% of
patients and muscular involvement is as high as 10%,
globally.
500
Pathology and Immunology:-
• Gastrointestinal symptoms are due to the
presence of the tape worm.
• Cysticercosis symptoms are a result of
inflammatory/immune responses.
• Antibodies are produced in cysticercosis and are
useful epidemiological tools.
501
Diagnosis:-
• Diagnosis is based on the recovery of eggs or proglottids in
stool or from the perianal area.
• Cysticercosis is confirmed by the presence of antibodies.
Treatment and control:-

• Praziquantel is the drug of choice.
• Expulsion of scolex must be assured to assume a satisfactory
treatment.
• A thorough inspection of beef and pork, adequate cooking
or freezing of meat is effective precautions, since cysticerci
do not survive temperatures below -10 oC and above 50oC.
502
2. Diphyllobothrium latum (fish or broad tapeworm)
Epidemiology:-
• Fish tapeworm infection is distributed

worldwide, in the subarctic and temperate
regions; it is associated with eating of raw
or improperly cooked fresh water fish.
503
Morphology:-
• This is the longest tapeworm found in man,
ranging from 3-10 meters with more than 3000
proglottids.
• The scolex resembles two almond-shaped leaves
and the proglottids are broader than they are
long, a morphology reflected in the organism's
name.
• Eggs are 30 x 50 micrometers in size and contain
an embryo with 3 pairs of hooklets (figure
below).
504
2. Diphyllobothrium latum (fish or broad tapeworm):
Morphology
505
2. Diphyllobothrium latum (fish or broad tapeworm): Morphology
506
2. Diphyllobothrium latum (fish or broad tapeworm): Morphology
507
Life cycle:-
• Man and other animals are infected by eating uncooked fish
that contains plerocercoid larvae (15 x 2 mm) which attach
to the small intestinal wall and mature into adult worms in 3
to 5 weeks.
• Eggs discharged from gravid proglottids in the small intestine
are passed in the feces.
• The egg hatches in fresh water to produce a ciliated
coracidium which needs to be ingested by a water flea
(Cyclops) where it develops into a procercoid larva.
• When infected Cyclops is ingested by the freshwater fish, the
procercoid larva penetrates the intestinal wall and develops
into a plerocercoid larva, infectious to man (figure below).
508
2. Diphyllobothrium latum (fish or broad tapeworm): Life Cycle
509
Symptoms:-
• Clinical symptoms may be mild, depending on
the number of worms.
• They include abdominal discomfort, loss of
weight, loss of appetite and some malnutrition.
• Anemia and neurological problems associated
with vitamin B12 deficiency are seen in heavily
infected individuals.
510
Diagnosis:-
• Diagnosis is based on finding many typical eggs and
empty proglottids in feces.
• A history of raw fish consumption and residence in
an endemic locality is helpful.
Treatment and control:-
• Praziquantel is the drug of choice.
• Freezing for 24 hours, thorough cooking or pickling
of fish kills the larvae.
• Fish reservoirs should be kept free of raw sewage.
511
3. Hymenolepis nana (dwarf tapeworm)
Introduction:-
• This is a small tapeworm (20 x 0.7 mm) which infects
children.
• Rodents are the reservoir.
• Infections are by the oro-fecal mode and, hence, cross
infection and auto infection by eggs in feces is normal
(figure 6).
• The worm develops from ingested eggs into an adult in
the small intestine and resides there for several weeks
(figure 5).
512
3. Hymenolepis nana (dwarf tapeworm)
Introduction:-
• Light infections produce vague abdominal disturbances
but heavier infections may cause enteritis.
• Diagnosis is based on finding eggs in the feces.
• Nicolsamide is the drug of choice.
• Hygiene is the best control.
513
3. Hymenolepis nana
• Three adult Hymenolepis
nana tapeworms.
• Each tapeworm (length:
15-40 mm) has a small,
rounded scolex at the
anterior end, and
proglottids can be
distinguished at the
posterior, wider end.
• Hymenolepis nana
adult
514
3. Hymenolepis sp
• Egg of Hymenolepis diminuta.
• These eggs are round or slightly
oval, size 70 - 86 µm X 60 - 80
µm, with a striated outer
membrane and a thin inner
membrane.
• The space between the
membranes is smooth or faintly
granular.
• The oncosphere has six hooks
(of which at least four are
visible at this level of focus).
515
3. Hymenolepis sp.
• Egg of Hymenolepis nana.
These eggs are oval or sub-
spherical and smaller than
those of H. diminuta, their size
being 40 - 60 µm X 30 - 50 µm.
• On the inner membrane are
two poles, from which 4-8
polar filaments spread out
between the two membranes.
• The oncosphere has six hooks
(seen as dark lines at 8
o'clock).
516
3. Hymenolepis nana
• Hymenolepis nana
cysticercoid
517
3. Hymenolepis nana : Life Cycle
• Eggs of Hymenolepis nana are immediately infective
when passed with the stool and cannot survive more
than 10 days in the external environment (1).
• When eggs are ingested by an arthropod intermediate
host(2) (various species of beetles and fleas may serve
as intermediate hosts), they develop into cysticercoids,
which can infect humans or rodents upon ingestion (3)
and develop into adults in the small intestine.
• A morphologically identical variant, H. nana var.
fraterna, infects rodents and uses arthropods as
intermediate hosts.
518
519
• When eggs are ingested (4) (in contaminated food or
water or from hands contaminated with feces), the
oncospheres contained in the eggs are released.
• The oncospheres (hexacanth larvae) penetrate the
intestinal villus and develop into cysticercoid larvae(5).
• Upon rupture of the villus, the cysticercoids return to
the intestinal lumen, evaginate their scoleces (6), attach
to the intestinal mucosa and develop into adults that
reside in the ileal portion of the small intestine
producing gravid proglottids (7).
• Eggs are passed in the stool when released from
proglottids through its genital atrium or when
proglottids disintegrate in the small intestine (8).
520
• An alternate mode of infection consists of internal
autoinfection, where the eggs release their hexacanth
embryo, which penetrates the villus continuing the
infective cycle without passage through the external
environment (9).
• The life span of adult worms is 4 to 6 weeks, but internal
autoinfection allows the infection to persist for years.
521
4. Echinococcosis (hydatid):-
INTRODUCTION:
– Echinococcus granulosus
and
– E. multilocularis
 Are causative agents of hydatid cysts.
522
4.1. Echinococcus granulosus
Epidemiology:-
• The organism is common in Asia, Australia,
and eastern Africa, southern Spain, southern
parts of South America and northern parts of
North America.
• The incidence of human infection about 1 to 2
per 1000 population and may be higher in
rural areas of affected regions.
523
4.1. E. granulosus: Morphology
• This is the
smallest of all
tapeworms (3
to 9 mm long)
with only 3
proglottids.
524
• "Hydatid sand".
• Fluid aspirated from a
hydatid cyst will shows
multiple protoscolices
(size approximately
100 µm), each of which
has typical hooklets.
• The protoscolices are
normally invaginated
(left), and evaginate
(middle, then right)
when put in saline
525
• Echinococcus granulosus
hydatid cysts in section of
lung
• Echinococcus granulosus
hydatid sand
526
• Echinococcus
granulosus egg
527
Hydatid cysts 528

• Histopathology of hydatid cyst. Echinococcus,
echinococcosis
529
• Histopathology of Echinococcus granulosus hydatid cyst
in a sheep. Thick fibrous pericyst, hyaline ectocyst, and
brood capsules filled with protoscolices are visible.
530
• Gross pathology of membrane and hydatid daughter
cysts from human lung
531
4.1. E. granulosus: Life cycle
• The adult worm lives in domestic and wild
carnivorous animals.
• Eggs, passed by infected animals, are ingested by
the grazing farm animals or man, localize in
different organs and develop into hydatid cysts
containing many larvae (proto-scolices or hydatid
sand) .
• When other animals consume infected organs of
these animals, proto-scolices escape the cyst,
enter the small intestine and develop into adult
worms.
532
• Echinococcus eggs, when swallowed by man, produce
embryos that penetrate the small intestine, enter the
circulation and form cysts in liver, lung, bones, and
sometimes, brain.
• The cyst is round and measures 1 to 7 cm in diameter,
although it may grow to be 30 cm.
• The cyst consists of an outer anuclear hyaline cuticula
and an inner nucleated germinal layer containing clear
yellow fluid.
• Daughter cysts attach to the germinal layer, although
some cysts, known as brood cysts, may have only larvae
(hydatid sand). Man is a dead end host.
533
534
• The adult Echinococcus granulosus (3 to 6 mm long) (1)
resides in the small bowel of the definitive hosts, dogs
or other canids. Gravid proglottids release eggs (2) that
are passed in the feces.
• After ingestion by a suitable intermediate host (under
natural conditions: sheep, goat, swine, cattle, horses,
camel), the egg hatches in the small bowel and releases
an oncosphere (3) that penetrates the intestinal wall
and migrates through the circulatory system into
various organs, especially the liver and lungs.
• In these organs, the oncosphere develops into a cyst (4)
that enlarges gradually, producing protoscolices and
daughter cysts that fill the cyst interior.
535
• The definitive host becomes infected by ingesting the
cyst-containing organs of the infected intermediate
host.
• After ingestion, the protoscolices (5) evaginate, attach
to the intestinal mucosa (6), and develop into adult
stages (1) in 32 to 80 days.
• The same life cycle occurs with E. multilocularis (1.2 to
3.7 mm), with the following differences: the definitive
hosts are foxes, and to a lesser extent dogs, cats,
coyotes and wolves; the intermediate host are small
rodents; and larval growth (in the liver) remains
indefinitely in the proliferative stage, resulting in
invasion of the surrounding tissues.
536
• With E. vogeli (up to 5.6 mm long), the definitive hosts
are bush dogs and dogs; the intermediate hosts are
rodents; and the larval stage (in the liver, lungs and
other organs) develops both externally and internally,
resulting in multiple vesicles.
• E. oligarthrus (up to 2.9 mm long) has a life cycle that
involves wild felids as definitive hosts and rodents as
intermediate hosts.
• Humans become infected by ingesting eggs (2), with
resulting release of oncospheres (3) in the intestine and
the development of cysts (4) in various organs
537
4.1. E. granulosus: Symptoms
• The symptoms, comparable to those of a slowly growing
tumor, depend upon the location of the cyst.
• Large abdominal cysts produce increasing discomfort.
• Liver cysts cause obstructive jaundice.
• Peribronchial cysts may produce pulmonary abscesses.
• Brain cysts produce intracranial pressure and Jacksonian
epilepsy.
• Kidney cysts cause renal dysfunction.
• The contents of a cyst may produce anaphylactic
responses.
538
4.1. E. granulosus: Diagnosis
• Clinical symptoms of a slow-growing tumor
accompanied by eosinophilia are suggestive.
• Intradermal (Casoni) test with hydatid fluid is
useful.
• Pulmonary cysts and calcified cysts can be
visualized using x-rays.
• Antibodies against hydatid fluid antigens have
been detected in a sizable population of infected
individuals by ELISA or indirect hemagglutination
test.
539
4.1. E. granulosus: Treatment & Control
• Treatment involves surgical removal of cyst or

inactivation of hydatid sand by injecting the cyst
with 10% formalin and its removal within five
minutes.
• It has been claimed that a high dose of
Mebendazole results in some success.
• Preventive measures involve avoiding contact
with infected dogs and cats and elimination of
their infection.
540
4.2. E. multilocularis
INTRODUCTION:-
• This is a tapeworm, similar to E. granulosus, that also
causes hydatid in northern parts of Asia and North
America.
• It has a very similar morphology and life cycle except
that rodents are its intermediate host.
• Humans, when infected with this worm, also develop
hydatid cysts which produce symptoms similar to those
caused by E. granulosus.
• However, the cysts are multilocular (many chambers).
• The organism is resistant to praziquantel; high doses of
Albendazole has some anti-parasitic effect.
• Surgery is the means of removing the cyst.
• Rodent control is the means of prevention.
541
542
543
TREMATODES
(FLUKES) 544
TREMATODES (FLUKES)
TEACHING OBJECTIVES
– Epidemiology, morbidity and mortality
– Morphology of the organism
– Life cycle, hosts and vectors
– Disease, symptoms, pathogenesis and site
– Diagnosis
– Treatment, prevention and control
545
TREMATODES (FLUKES)
INTRODUCTION:-
• The most significant trematodes from a clinical point
of view are
1. Blood flukes,
– Schistosoma mansoni,
– S. japonicum and
– S. hematobium.
• Other trematodes of significance are
2. Intestinal fluke,
– Fasciolopsis buski,
3. Liver fluke,
– Clonorchis sinensis and
4. Lung fluke,
– Paragonimus westermani.
546
1. Schistosomiasis (Bilharziasis)
Introduction:-
• The three species of Schistosoma have different
geographic distributions.
– S. hematobium is prevalent in Africa,
– S. mansoni is found in Africa and America and
– S. japonicum is common in the far east.
Epidemiology:-
• Approximately 250 million people are infected
with schistosomes and 600 million are at risk
547
1. Schistosomiasis (Bilharziasis)
Morphology:-
• Adult worms are 10 to 20 mm long; the male has
an unusual lamelliform shape with marginal folds
forming a canal in which the slender female
worm resides.
• Unlike other trematodes, schistosomes have
separate sexes (figure 1).
548

Advanced Parasitology Lecture1, Introduction

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Advanced Parasitology Lecture1, Introduction

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PRINCIPLES OF PARASITOLOGY

• Zoology, with its emphasis with identification and classification of

• Between some animals, however, a variety of patterns of association have

• Homogenetic associations ­those between individuals of the same

 Individuals of the same species may form loosely united communities,

2.COMMENSALISM:The term literally means 'eating at the same table‘.

Examples: Clown Fish and sea-anemone: The sea anemone provides

a) the intimacy of the association,

b) its pathogenic effect,

c) its metabolic or physiological dependence,

d) whether or not the host 'recognizes' the parasite as 'foreign',

e) the ability of the parasite to 'recognize' the host site as being a

ii. The parasite is physiologically or metabolically dependent upon its

iii. Heavily infected hosts will be killed by their parasites.

v. There is an over dispersed frequency distribution of parasites within the

What we mean by metabolic dependance?

– penetrates external openings - buccal cavity, cloaca, external ear

– Eukaryotic microparasites are primarily protozoans

– Are incapable of surviving outside the host environment (naturally

– These parasites of parasites are called hyperparasites

– Hyperparasites are usually bacteria or viruses, but some protozoans,

 Aberrant Parasite– In an usual host or location 21

– can be a definitive or an intermediate host, depending on whether the

 Paratenic (transport) host:- optional transport host - no detectable

– Serving as a source of infection for others

 Infection: – Parasites (endoparasites) inside a host

 Infestation: – Parasites (ectoparasites) on a host

 Infection vs Disease (-iasis, -osis, -os) : clinical or subclininical

• Parasites may occur without causing disease

 The essence of parasitism rests with the nature of host-parasite relationships

 Parasitism is an ecological concept i.e is essentially a branch of ecology in

• The phenomenon of parasitism can be considered as an ecological

• Because dealing with parasites and their hosts from an ecological

– Examples:- alimentary canels or gills of fishes. It is possible that two

The less common ones in vertebrates:

• The physioco-chemical conditions of a habitat

Parasites cause disease in man by:

– Sterilizing immunity preventing new infection, as in

– The immune response by the host is usually specific to

• Protozoa, like other eukaryotic cells, have a

Fig. 1.46 Trypanosoma

Fig. 1.48 Entamoeba histolytica has an

• Some protozoa, such as the extracellular stages

• Classification of the subkingdom Protozoa

• There are four phyla of protozoa of Medical and

– Entamoeba histolytica (Amebae)

– 0.5 to 50% of the population world wide harbors E.

Gross pathology of amebic abscess

• There is an antibody response after invasive

• Iodoquinol is used to treat asymptomatic

• Metronidazole is used for symptomatic and

• These cysts have two nuclei each (more

Giardia lamblia cyst, Iodine stain 110

DAPI staining Indirect fluorescent

of giardia antibody stain

G. lamblia Infection in Human Intestine

 Covering of the intestinal epithelium by the

 There is increased incidence of infection in

• a bean shaped macronucleus which

Oocysts of C.parvum stained

• When excreted, they are immature

• The oocyst matures after excretion:

T. vaginalis – Vaginal discharge

• Trophozoites must be distinguished from the

• Homogenetic associations those between individuals of the same