1

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PROTOZOA
Protozoa 2

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Protozoa are single celled non
photosynthetic eukaryotic
organisms
They are unicellular heterotrophs
They lack cell wall and are
motile or non motile
Introduction 3

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They have a thin layer supporting
the cell membrane called have
pellicle. This is purposed for
protection and to retain their
shape, especially during locomotion
Pellicles allow the organism to be
more hydrodynamic
Introduction 4

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Protozoa obtain energy from
organic substance
They are aerobics or facultative
anaerobes
Protozoa may take in food by
osmotrophy, absorbing nutrients
through their cell membranes; or
Introduction 5

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 Detailed features of protozoa can be
seen with an electron microscope
 Protozoa are free living and can be
symbionts or parasites
Classification of protozoa 6

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Protozoa have been divided based on their means of locomotion.
 Mastigophora - move with the help of whip-like structures called
flagella (e.g., Giardia lamblia, trypanosoma)
 Ciliophora - move by using hair-like structures called cilia(e.g.,
Balantidium coli)
Classification 7

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 Sporozoas- non motile, no cilia or flagella e.g Plasmodium
falcipurum, P. ovale, P. malarae, P. vivax
 Sarcodina - move by the use of false feet called pseudopodia
(e.g., Entamoeba histolytica)
Protozoan diseases 8

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Some protozoa are human parasites,
causing diseases including

 Malaria
 Giardiasis
 Toxoplasmosis
 Trichomoniasis
 9

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 Chagas disease,
 Leishmaniasis,
 Sleeping Sickness,
 Amoebic dysentery.
Transmission 10

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 Transmissionof intestinal protozoa
occurs through a fecal-oral route
 Protozoa that live in the blood or
tissue of humans are transmitted by
arthropod vector such as bite of a
mosquito
Treatments 11

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 Antimicrobials
including Daraprim
(pyrimethamin) Flagyl
(metronidazole) e.t.c are used in
treatment of protozoan infections
 12

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Other Protozoa
PLASMODIAL INFECTIONS (MALARIA)
13
Phylum: Protozoa

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Sub-phylum: Apicomplexa
(Sporozoa)
Infective agent:
Plasmodium falciparum,
P. malariae,
P. ovale,
P. vivax
INTRODUCTION 1
14

Malaria is a vector borne

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disease and the most
important parasitic disease
of man.

Itis a protozoan infection of

the RBC’s and is transmitted
by the blood feeding female
Anopheline mosquitoes.
15

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Plasmodium falciparum 16

Causes malignant tertian

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malaria with 36 – 48hr cycle
parasitedensity exceed
250,000 – 300,000 / µl of blood
Covers a large geographical
range and is the most
pathogenic of all four species.
(Generally confined to the
tropics)
Plasmodium vivax
17
Causes benign tertian

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malaria with a 48hr cycle.

Itcovers a large geographic

range, more common in
South America, N. Africa,
India but rare in South
Saharan Africa.
It tends to have a “true 18
relapse” from the residual

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liver stages.

It infects young RBC’s.

Parasitedensity rarely
exceed 50,000 / µl of
blood.
Plasmodium ovale 19
Causes benign tertian malaria

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with a 48hr cycle.
It covers a narrow geographic
range (rare out side West
Africa and South Pacific
islands/ regions)
It infects young RBC’s
Plasmodium malariae
20

Is
responsible for quartan

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malaria with a 72hr cycle.
Itcovers a narrow
geographic range; it is
sporadic in distribution but
relatively uncommon
outside Africa.

Itis associated with 21
recrudescence and “nephrotic
syndrome” with no true

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relapse.
P.vivax and P. malariae infect
about 1 – 2% or less RBC’s, P.
ovale infects less than 2% of
RBC’s.
P.falciparum infects or
parasites up to 30 – 40%.
Almost all deaths due to 22
malaria and severe

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complications are caused by P.
falciparum
The other three parasites
cause benign malarias, severe
disease condition is unusual,
however, occasionally patients
may die from rapture of an
enlarged spleen
EPIDEMIOLOGY 1
23
A) THE VECTOR

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Themain vector is the
female Anopheles mosquito

Temperatures below 16 0C or
above 33 0C tend to prevent
the sporogonic cycle in the
mosquito (takes 2 wks).
Transmission is 24
proportional to the

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1. Density of the vector
2. Number of times of bites
each day
3. The survival of the
vector after feeding
 Vectors differ in their natural 25
density (abundance)/ feeding /
resulting behaviors / breeding site

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preferences / flight ranges / choice
of food (blood) / vulnerability to
environmental conditions and
insecticides.

 Anopheles gambiae is the most

infective vector / are tough /
long lived / naturally occur in high
densities / bite humans frequently.
EPIDEMIOLOGY 3 26
B) THE HUMAN HOST

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Human behaviour plays a
major role in the
transmission of malaria.

There is the need for human

reservoir of gametocytes to
transmit the infection.
 Inareas of high transmission,
27
infants/young children are most
susceptible than adults

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 Parasitedensities tend to be
higher in children and
gametocytes tend to be detected
more frequently in children.
 Theyounger age groups usually
represent the main reservoir
group and the main recipients of
infection.
Children who survive 28
infection achieve a state of

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premunition where
infections cause little or no
problems to host (children).

Premunition is therefore a
form of immunity that
develops to control but not
to prevent infection.
Falciparum malaria infections
29
are more severe in pregnancy
and infrequent in babies.

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Factors responsible for
infrequent malaria in infants
include passive transfer of
matenal immunity and high
haemoglobin F content of
infants’ erythrocytes, which
retard parasite development.
LIFE CYCLE 1
30
Cycle is complex, consists
of two main stages:

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A) Human Stages

1) Pre-erythrocytic
schizogony
2) Erythrocytic schizogony
3) Erythrocytic
gametogony
 B) Mosquito Stages 31

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1)Fertilization, meiosis and ookinete
formation
2) Formation of oocysts and
sporogony

 Malaria provides an example of

stage - development specificity of
invasion.
e.g. sporozoites – liver cells
merozoites – RBC’s
Life cycle of Malaria parasites
32

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LIFE CYCLE 3
33
 A) PRE-ERYTHROCYTIC (Hepatic Phase)

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Begins when the female
anopheles mosquito
inoculates plasmodial
sporozoites into the blood
stream of man
These small motile
sporozoites may be few in
the inoculum (8 – 15) or can
Sporozoites enter the 34
circulation either directly or

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through the lymph channels
and home to the liver
parenchyma cells.

Thishappens between
(within) 45min all
sporozoites would have
entered the liver or have
been cleared.
The sporozoites live in 35
the hepatocytes (liver

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cells) and begin asexual
(schizogonic)
reproduction.

Schizogonic phase can

last between 5 days (P.
falciparum) to 15 days for
(P. malariae)
  In P. vivax and P. ovale infections, a
36
proportion of the intrahepatic parasites
do not develop but go into a state of

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rest
(quiescence) referred to as the
hypnozoites
(latent forms) which become active
weeks
/ months later.
 These quiescent stages (sleeping
stages) are responsible for relapses
which characterize those P. vivax / P.
ovale infections.
During this asexual phase 37
(schizogony), multiplication

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occur producing many
thousands of merozoites
which are released from
ruptured infected
hepatocytes.

This phase is asymptomatic

for the human host.

38
B) ASEXUAL BLOOD STAGE DEVELOPMENT

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Erythrocytic schizogonic
phase
Erythrocytic gametogonic
phase

Released merozoites rapidly

invade red cells.
Attachment of parasite to
RBC is facilitated by specific
 In P. vivax - the duffy blood
e.g. 39
group antigen Fya or Fyb 29,
30 . This antigen is absent in

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West Africans and this explains
absence of P. vivax infection in
the region

Receptors to P. falciparum have

been identified as glycophorins
but receptors for P. malariae
and P. ovale are not known.
On entry the merozoites 40
undergo several morphological
changes and development from

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Ring Forms (trophozoites) 
Schizonts  Merozoites

Inthe early stages (less than

12hrs) the ring forms of all 4
species appear to be identical
under the microscope.
Ring forms of P. falciparum look 41
like signet ring or a pair of
earphones with darkly stained

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chromatin in the nucleus, a
circular rim of cytoplasm and a
central vacuole – they are motile.

As they grow – they consume the

contents of the erythrocytes,
usually the haemoglobin.
 42

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Ring forms of P.
falciparum in
RBCs
In 43
about 24 – 26hrs of
development, P. falciparum

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exhibits a high molecular
weight strain variant antigen
on the surface of infected RBCs
(knob-like projections)

These structures facilitate

attachment to vascular
endothelium.
These RBCs disappear from 44
circulation (sequestration) and
attach to the walls of the

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vessels (cytoadherence)a
process called.

The other 3 species (benign

malaria) do not cyto-adhere
and all stages of these
parasites are found in the
peripheral blood.
P.vivax during growth 45
enlarges the infected RBC

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leading to the appearance of
red granules (pigments)
throughout the RBC called
Schüffners dots. These are
also found in P. ovale.

P.malariae produces
characteristic band forms as
parasites nature.
Infected RBCs rupture 46
releasing merozoites

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between 6 and 36 per RBC.

Asexual life cycle is 48 hrs

(tertian malaria) for P.
falicparum, P. vivax, P.
ovale and 72hrs (quartan
malaria for P. malariae)
C) POST ERYTHROCYCTIC STAGE SEXUAL STAGES AND
DEVELOPMENT IN THE MOSQUITO 47

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 After series of asexual
cycles, a sub population of
parasites develop (by
gametogomy) into sexual
forms (gametocytes), which
are long lived and motile.
Theprocess of gametogony 48
takes 4 days in P. vivax

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infections and more than 10
days in P. falciparum.

Upon ingestion of male and

female gametocytes the
parasites become activated
and develop, multiply and
fuse to form a zygote.
Male and Female gametocytes of 49
P. falciparum

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Within 24hrs the enlarging 50
zygote (ookinete) becomes

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motile and penetrates the
walls of the mosquito’s mid gut
(stomach) where it encysts as
an oocyst.

The oocyst finally raptures to

release myriads of sporozoites
into the coelomic cavity of the
mosquito.
These sporozoites then 51
migrate to the salivary
glands ready for

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inoculation into the next
host

Sporogony and takes

between 8 – 35 days
depending on ambient
temperature / species of
parasites / mosquito.
HUMAN GENETICS AND MALARIA
52

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Genetic polymorphism of
several human genes affect
– entry / multiplication
/survival / development of
malaria parasites and this
determines the outcome of
the infection.
Parasite invasion of RBC’s 53
depends on specific surface

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molecules on the RBC’s
For P. vivax – duffy
antigens
For P. falciparum –
glycophorin A

Most black African are duffy

antigen negative but not
Malaria is seldomly found 54
in carriers of the sickle cell

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trait (HbS or AS)

P.falciparum infected RBCs

adhere to the walls of
blood vessels via knobs
that form as parasites
mature in RBC’s (infected)
This sequestration causes 55
the infected or parasitised

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RBCs to hide in areas of
reduced O2 tension which
then facilitates sickling /
potassium loss and killing of
the parasite.
Other genetic abnormalities 56
that restrict the growth of
malaria parasites within RBC’s

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are
G6PD – deficiency and
Thalassaemia

 In this case there is a reduced

ability for the RBC’s to produce
NADPH via the pentose
phosphate shunt, this results
in an oxidative stress, which
Also certain human leucocyte 57
antigens (HLAS) common in
West African also confer

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protection against severe
malaria.

Class 1 antigen HLA – BW53

and
Class 2 antigen HLA –
DRB1.1302
PATHOGENESIS AND CLINICAL MANIFESTATIONS 1 58

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The disease could be
uncomplicated or complicated.
The main manifestations of
malaria are fever, chills and
anaemia.
The typical malarial paroxysm
coincides with the
simultaneous lysis of many
There are 4 main processes. 59

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1. Fever – the basis remain
abscure

2. Anaemia
a. Haemolysis
b. Sequestration of
infected RBC’s in the
3. Tissue Hypoxia – 60
Resulting from anaemia and

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alteration in the microcirculation:-
pulmonary oedema, renal failure,
cerebral dysfunction.

 4. Immunologic Events
These include hypoglobulinaemia;
antibody mediated splenic
sequestration of platelets,
immune complex disease,
CLINICALLY
61
 The first symptoms are non-specific and resemble

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influenza and are similar for all 4 species. Non-
specific signs and symptoms include:

 Fever (periodic, paroxysms) – headaches, muscular

ache / vague abdominal discomfort / lethargy /
lassitude and dysphoria / temperature rise / loss of
appetite, chills, hepatomegaly and anaemia, joint
pains, sweating.
 SPECIES – Specific syndromes
62
P. vivax and P. ovale – fever and

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anaemia debilitate the
patient but is unusual.

P. malariae – mortality is rare, it

is most often associated with
immune complex disease
including an irreversible
glomerulonephritis in children
in endemic areas.
 63
P.falciparum – can
cause lethal

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complications especially
in non immune persons
and pregnant women.
 Other complications associcted 64
with severe P. falciparum
infections include:

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Cerebral malaria
Hypoglycemia (especially in
pregnant women)
Renal failure from acute
tubular necrosis
Massive intracellular
haemolysis (black water
fever)
Pulmonary oedema
DIAGNOSIS
65
 Microscopic identification of parasites in blood is the
most certain method

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 Usually thin and thick blood films are prepared

 The thick film is examined to detect the presence of

the parasites

 The thin film is examined to identify the species and

to give estimate of the level of parasitaemia

 The films are stained in Giemsa’ stain or

Leishman’s, or Field’s stains
ESTIMATION OF NUMBER OF PARASITES 66

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 1 – 10 per 100 high power field --- + (1+)
 11 – 100 per “ “ “ --- ++ (2+)
 1 – 10 in every high power field--- +++ (3+)
 more than 10 in every high power field-- ++++ (4+)
PREVENTION AND CONTROL 67

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 Avoiding mosquito bites
 Use of drugs
 Prevention of mosquito breeding
 Elimination of all adult mosquitoes
 Health education
 Immunization
TREATMENT
Available antimalarials are in 3 broad groups 68

1. Quinoline-related Compounds

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Quinines, quinidine, chloroquine, amodiaquine,
mefloquine, Halofantrine, primaquine.
2. Antifols
Prymethamine, proguanil, chlorproguanil,
trimethoprim
3. Artemisinin Compounds
Artemisinin, artemether, artesunate

 Of these three groups, the Artemisinin compounds

have the broadest time window of action on asexual
malaria parasites from medium sized rings to early
shizonts.