Protozoans
Protozoans include a wide diversity of taxa that
do not form a monophyletic group but all are
unicellular eukaryotes.
Protozoa lack a cell wall, have at least one
motile stage in their life cycle and most ingest
their food.
Protozoan cell is much larger and more complex
than prokaryotic cell and contains a variety of
organelles (e.g. Golgi apparatus, mitochondria,
ribosomes, etc).
Protozoans
Eukaryotic cell was developed through endosymbiosis.
In distant past aerobic bacteria appear to have been
engulfed by anaerobic bacteria, but not digested.
Ultimately, the two developed a symbiotic relationship
with the engulfed aerobic bacteria becoming
mitochondria and eukaryotic cells developed.
In a similar fashion, ancestors of chloroplasts formed
symbiotic union with other prokaryotes.
Protozoans
Protozoans include both autotrophs and
heterotrophs. They include free-living and
parasitic forms.
Reproduction can be asexual by fission or
budding or sexual by conjugation or
syngamy (fusion of gametes).
Protozoans
The protozoa were once considered a
single phylum, now at least 7 phyla are
recognized.
Were also once grouped with unicellular
algae into the Protista, an even larger
paraphyletic group.
Figure 11.01
Movement in Protozoa
Protozoa move mainly using cilia or
flagella and by using pseudopodia
also used for feeding in many small
Cilia
metazoans.
Cilia and flagella
No real morphological distinction between
the two structures, but cilia are usually
shorter and more abundant and flagella
fewer and longer.
Each flagellum or cilium is composed of 9
pairs of longitudinal microtubules arranged
in a circle around a central pair.
Cilia and flagella
The collection of tubules is referred to as
the axoneme and it is covered with a
membrane continuous with the rest of the
organism’s cell membrane.
Axoneme anchors where it inserts into the
main body of the cell with a basal body.
Figure 11.09a
Protein spoke
Dynein motor
Basal body
Cilia and flagella
The outer microtubules are connected to
the central pair by protein spokes.
Neighboring pairs of outer microtubules
(doublets) are connected to each other by
an elastic protein.
Figure 11.09a
Protein spoke
Dynein motor
Cilia and flagella
Cilium is powered by dynein motors on the outer
doublets. As these motors crawl up the adjacent
doublet (movement is powered by ATP) they
cause the entire axoneme to bend.
The dynein motors do not cause the doublets to
slide past each other because the doublets are
attached to each other by the elastic proteins
and the radial spokes and have little freedom of
movement up and down. Instead the walking
motion causes the doublets to bend.
Flagella, “intelligent design” and
irreducible complexity
the humble flagellum has been
Oddly,
dragged into the evolution culture wars!
Flagella, “intelligent design” and
irreducible complexity
The U.S. Supreme Court has prohibited
the teaching of creationism in public
schools as a violation of the
“establishment of religion” clause of the
constitution.
attempt to insert creationism into
Latest
schools is the idea of “Intelligent Design.”
Flagella, “intelligent design” and
irreducible complexity
The concept of “intelligent design” is outlined
most clearly in Michael Behe’s book “Darwin’s
Black Box.”
The central idea in “intelligent design” is that
some structures in the body are so complex that
they could not possibly have evolved by a
gradual process of natural selection. These
structures are said to “irreducibly complex.”
Flagella, “intelligent design” and
irreducible complexity
By “irreducibly complex” Behe means that
a complex structure cannot be broken
down into components that are
themselves functional and that the
structure must have come into existence in
its complete form.
Flagella, “intelligent design” and
irreducible complexity
Ifstructures are “irreducibly complex”
Behe claims that they cannot have
evolved.
Thus, their existence implies they must
have been created by a designer (i.e. God,
although the designer is not explicitly
referred to as such).
Flagella, “intelligent design” and
irreducible complexity
One of Behe’s main examples is flagella/cilia.
Behe claims that because cilia are composed of
at least half a dozen proteins, which combine to
perform one task, and that all of the proteins
must be present for a cilium to work and that
cilia could not have evolved in a step-by step
process of gradual improvement.
Flagella, “intelligent design” and
irreducible complexity
The flagellum is not, in fact, irreducibly complex.
For example, the flagellum in eel sperm lacks
several of the components found in other flagella
(including the central pair of microtubules, radial
spokes, and outer row of dynein motors), yet the
flagellum functions well.
Flagella, “intelligent design” and
irreducible complexity
The whole “irreducible complexity”
argument could in reality be recast as an
argument of “personal incredulity.”
“Ipersonally cannot imagine a sequence
of steps by which this complex structure
could have evolved. Therefore, it must
have been created.”
Movement in Protozoa:
Pseudopodia
Pseudopodia are chief means of
locomotion of amoebas but are also
formed by other protozoa and amoeboid
cells of many invertebrates.
Inamoeboid movement the organism
extends a pseudopodium in the direction it
wishes to travel and then flows into it.
Pseudopodia
Amoeboid movement involves endoplasm and
ectoplasm. Endoplasm is more fluid than
ectoplasm which is gel-like.
When a pseudopodium forms, an extension of
ectoplasm (the hyaline cap) appears and
endoplasm flows into it and fountains to the
periphery where it becomes ectoplasm. Thus, a
tube of ectoplasm forms that the endoplasm
flows through. The pseudopodium anchors to
the substrate and the organism moves forward.
Figure 11.10
Feeding in amebas
Feeding in amoebas involves using
pseudpodia to surround and engulf a
particle in the process of phagocytosis.
Theparticle is surrounded and a food
vacuole forms into which digestive
enzymes are poured and the digested
remains are absorbed across the cell
membrane.
Phagocytosis
Reproduction in protozoa
The commonest form of reproduction is
binary fission in which two essentially
identical individuals result.
In some ciliates budding occurs in which
a smaller progeny cell is budded off which
later grows to adult size.
Binary fission
in various taxa
Sexual reproduction in protozoa
All protozoa reproduce asexually, but sex
is widespread in the protozoa too.
In ciliates such as Paramecium, a type of
sexual reproduction called conjugation
takes place in which two Paramecia join
together and exchange genetic material
Figure 11.28
Diseases caused by protozoa
Many diseases are caused by protozaon
parasites
These include:
Malaria (caused by a sporozaon)
Giardia, Sleeping sickness (caused by
flagellates)
Amoebic dysentry (caused by amoebae)
Malaria
Malaria is one of the most important diseases in the
world.
About 500 million cases and an estimated 700,000 to
2.7 million deaths occur worldwide each year (CDC).
Malaria was well known to the Ancient Greeks and
Romans. The Romans thought the disease was caused
by bad air (in Latin mal-aria) from swamps, which they
drained to prevent the disease.
Malaria symptoms
The severity of an infection may range from
asymptomatic (no apparent sign of illness) to the
classic symptoms of malaria (fever, chills,
sweating, headaches, muscle pains), to severe
complications (cerebral malaria, anemia, kidney
failure) that can result in death.
Factors such as the species of Plasmodium and
the victims genetic background and acquired
immunity affect the severity of symptoms.
Malaria
Despite humans long history with malaria
its cause, a sporozoan parasite called
Plasmodium, was not discovered until
1889 when Charles Louis Alphonse
Laveran a French army physician
identified it, a discovery for which he won
the Nobel Prize in 1907.
Malaria
In1897 an equally important discovery,
the mode of transmission of malaria, was
made by Ronald Ross.
His identification of the Anopheles
mosquito as the transmitting agent earned
him the 1902 Nobel Prize and a
knighthood in 1911.
Plasmodium
There are four species of Plasmodium: P.
falciparum, P. vivax, P.ovale and P.
malariae.
falciparum causes severe often fatal
P.
malaria and is responsible for most
deaths, with most victims being children.
Plasmodium
Both Plasmodium vivax and P. ovale can go
dormant, hiding out in the liver. The parasites
can reactivate and cause malaria months or
years after the initial infection.
P. malariae causes a long-lasting infection. If
the infection is untreated it can persist
asymptomatically for the lifetime of the host.
Life cycle of malaria
Plasmodiumhas two hosts: mosquitoes
and humans.
reproduction takes place in the
Sexual
mosquito and the parasite is transmitted to
humans when the mosquito takes a blood
meal.
Life cycle of malaria: humans
The mosquito injects Plasmodium into a human in the
form of sporozoites.
The sporozoites first invade liver cells and asexually
reproduce to produce huge numbers of merozoites
which spread to red blood cells where more merozoites
are produced through more asexual reproduction.
Some parasites transform into sexually reproducing
gametocytes and these if ingested by a mosquito
continue the cycle.
Plasmodium gametocyte
Life cycle of malaria: mosquitoes
Gametocytes ingested by a mosquito combine in
the mosquito’s stomach to produce zygotes.
These zygotes develop into motile elongated
ookinites.
The ookinites invade the mosquito’s midgut wall
where they ultimately produce sporozoites,
which make their way to the salivary glands
where they can be injected into a new human
host.
How Plasmodium enhances
transmission rates
ThePlasmodium parasite engages in a
number of manipulative behaviors to
enhance its chances of being transmitted
between hosts.
Such manipulations are a common feature
of parasite behavior, in general, as we will
see throughout the semester.
How Plasmodium enhances
transmission rates
Mosquitoes risk death when feeding and
attempt to minimize risk and maximize
reward when doing so.
Toobtain blood a mosquito must insert its
proboscis through the skin and then locate
a blood vessel. The longer this takes, the
greater the risk.
How Plasmodium enhances
transmission rates
As soon as the mosquito hits a blood
vessel the host’s body responds by
clotting the wound.
Plateletsclump around the proboscis and
release chemicals which cause the
platelets to clot together.
How Plasmodium enhances
transmission rates
To slow clotting and speed feeding, mosquitoes
inject anticoagulants including one called
apyrase that unglues the platelets. They also
inject other chemicals that expand the blood
vessels.
Plasmodium in the host helps the mosquito feed
by releasing chemicals that also slow clotting.
The parasite’s help increases the chances of the
mosquito feeding successfully and sucking up
the parasite.
How Plasmodium enhances
transmission rates
Once in the mosquito Plasmodium needs about
10 days to produce sporozoites that are ready to
be injected into a human.
During this time, to reduce the chances of the
mosquito dying, Plasmodium apparently
discourages its host from eating. Although how
the parasite does this is not clear, mosquitoes
containing ookinites abandon feeding attempts
sooner than parasite-free mosquitoes.
How Plasmodium enhances
transmission rates
Once sporozoites are in the salivary
glands, however, Plasmodium wants the
mosquito to bite and bite often.
Inthe salivary gland the parasite cuts off
the mosquito’s anticoagulant apyrase
supply. This makes it harder for the
mosquito to feed so it is hungrier and bites
more hosts.
How Plasmodium enhances
transmission rates
As a result, an infected mosquito is twice
as likely to bite two people in a single night
as an uninfected mosquito is.
Asa result, the parasite is spread more
widely.
Behavior of Plasmodium in humans
Plasmodium enters the blood stream through a
mosquito bite.
The parasite must avoid the host’s immune
system. To do so while in the body it moves
from one hiding place to another.
The parasite moves first to the liver. Can get
there in about 30 minutes, which is usually fast
enough to avoid triggering the immune system.
Behavior of Plasmodium in humans
At the liver Plasmodium enters a liver cell.
The cell responds by grabbing
Plasmodium proteins and displaying the
antigens on its cell surface in a special cup
the major histocompatibility complex or
MHC.
Behavior of Plasmodium in humans
Theimmune system recognizes the
Plasmodium antigens and mounts an
immune response.
However, in a week before the immune
system has mounted its full response the
parasite has produced about 40,000
copies of itself and these burst out of the
liver to seek red blood cells.
Behavior of Plasmodium in humans
Theparasites leave the liver, reenter the
bloodstream, and find a red blood cell to
enter.
Eachparasite spends two days in a red
blood cell consuming the hemoglobin and
reproducing.
Plasmodium in red blood cell
Red blood cells
Red blood cells (strictly red blood
corpuscles) are a challenging environment
to live in.
They lack a nucleus and have little
metabolic activity. As a result, they have
few proteins for generating energy and
also lack most of a normal cell’s channels
for transporting fuel in and wastes out.
Red blood cells
Red blood cells are specialized to
transport oxygen, which they carry by
binding and wrapping in hemoglobin
molecules.
A red blood cell is pumped around the
body by the heart and travels about 300
miles over its lifetime.
Red blood cells
Red blood cells are squeezed through
slender capillaries and compressed to one
fifth of their normal diameter before
rebounding.
To survive this squeezing, red blood cells
have a network of proteins under their
membrane that can fold like a concertina
and allow the cell to stretch and squeeze
as needed.
Red blood cells
Oldred blood cells eventually lose their
elasticity and become stiff.
Those that show signs of such aging are
filtered out as they pass through the
spleen and destroyed.
Behavior of Plasmodium in humans
Plasmodium cannot swim but uses hooks
to move along the blood vessels.
Atthe parasite’s tip are sensors that
respond only to young red blood cells and
clasp on to proteins on the cell’s surface.
Behavior of Plasmodium in humans
The parasite uses a set of organelles
concentrated at its apical end to gain
entry. A suite of proteins are produced
that cause the red blood cell’s membrane
to open and let the parasite squeeze in.
takes only about 15 seconds for the
It
parasite to get in.
Figure 11.30
Plasmodium Sporozoite
Behavior of Plasmodium in humans
Inside in the red blood cell the
Plasmodium consumes the hemoglobin. It
takes in a small amount of hemoglobin,
slices it apart with enzymes and harvests
the energy released.
The toxic core of the hemoglobin molecule
is processed into an inert molecule called
hemozoin.
Behavior of Plasmodium in humans
In order to reproduce, Plasmodium needs more
than hemoglobin.
It sets about modifying the red blood corpuscle
so it can obtain amino acids and make proteins.
The parasite builds a series of tubes that
connect it to the surface of the cell and uses
these to bring in materials from the blood steam
and to pump out wastes.
Behavior of Plasmodium in humans
The parasite also produces proteins that help to
maintain the red blood cell’s springiness for as
long as possible so it is not eliminated by the
spleen.
After a few hours, however, the red blood cell
has been too modified by the parasite to fool the
spleen. The parasite now produces sticky latch
proteins that glue the cell to blood vessel walls.
Behavior of Plasmodium in humans
Infected cells clump up in capillaries.
After another day the contents of the cell have
been used up. The cell ruptures and 16 new
parasites burst out to infect other red blood cells.
Some of these parasites transform into sexually
reproducing gametocytes and, as mentioned
previously, these if ingested by a mosquito will
continue the cycle.
Behavior of Plasmodium in humans
While in the red blood cells Plasmodium is
invisible to the immune system because
the red blood cells have no MHC and
cannot alert the immune system.
The latch proteins however do stimulate
the immune system.
Behavior of Plasmodium in humans
The latch protein is made by a single
gene, but Plasmodium has over 100 such
genes each of which produces a unique
latch.
Ineach generation some of the new
parasites switch on a new latch gene and
so the immune system is always playing
catch up.
Effects of malaria on human
evolution
Theintense selection pressure imposed
by malaria has resulted in a large number
of mutations that provide protection
against the parasite being selected for in
humans.
The best known is sickle cell anemia.
Anti-malaria mutations: Sickle cell
anemia
Sicklecell anemia is a condition common
in West Africans (and African Americans
of West African ancestry).
In sickle cell anemia red blood cells are
sickle shaped as a result of a mutation
which causes hemoglobin chains to stick
together.
Anti-malaria mutations: Sickle cell
anemia
People with the sickle cell allele are protected
against Plasmodium because their hemoglobin
under low oxygen conditions contracts into
needle-shaped clumps.
This contraction not only causes the sickling of
the cell, but harms the parasite. Parasites are
impaled on the clumps and the cell loses its
ability to pump potassium, which the parasite
needs.
Anti-malaria mutations: Sickle cell
allele
People with two copies of the sickle cell
allele usually die young, but heterozygotes
are protected against malaria.
Asa result the geographic distribution of
the allele and malaria in Africa match quite
closely.
Anti-malaria mutations: (G6PD)
deficiency
Glucose-6-phosphate dehydrogenase
(G6PD) deficiency. There are hundreds
of alleles known and with more than 400
million people affected G6PD deficiency is
the commonest enzyme deficiency known.
Anti-malaria mutations:
Thalassemia
Geographic distribution suggests it
protects against malaria and
epidemiological evidence also supports
this.
People with G6PD-202A a reduced activity
variant common in Africa have a
significantly reduced risk of suffering
severe malaria.
Anti-malaria mutations:
Thalassemia
Thalassemia:People with thalassemia
make the ingredients of hemoglobin in the
wrong amounts.
Toomany or too few α or ß hemoglobin
chains are produced and when they are
assembled into hemoglobin molecules
spare chains are left over.
Other anti-malaria mutations:
Thalassemia
Extra chains clump together and cause major
problems in the cell. These clumps grab oxygen,
but don’t enclose it and the oxygen often
escapes and because it is strongly charged, the
oxygen damages other molecules in the cell.
Severe thalassemia is fatal, but mild forms
protect against malaria because the loose
oxygen severely damages the parasite and
renders it unable to invade new cells.
Anti-malaria mutations:
Ovalocytosis
Ovalocytosis: Occurs in South east Asia and
has same genetic rules and consequences as
sickle cell anemia.
People with ovalocytosis have blood cell walls
that are so rigid they can’t slip through
capillaries. The rigid cell walls make it hard for
the parasite to enter the cell and the cell’s rigidity
appears to prevent the parasite pumping in
phosphates and sulphates it needs to survive.
Anti-malaria mutations:
One major advantage of these various anti-
malarial mutations appears to be that they
provide a natural vaccination program for
children.
By slowing the development of the parasite
these mutations give a child’s naïve immune
system time to overcome Plasmodium’s
attempts to elude the immune system and mount
an immune response. Mild cases of malaria
thus immunize children to malaria and allow
them to survive to adulthood.
Mosquito nets save lives
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nets.
Human African Trypanosomiasis
(Sleeping sickness)
Sleeping sickness is a protozoan disease, which
like malaria is spread by an insect vector, the
tsetse fly.
The disease is endemic to sub-Saharan Africa
and an estimated 300,000 people are infected
annually with about 40,000 deaths.
The disease organism is Trypanosoma brucei.
Trypanosoma forms in blood smear from patient with African trypanosomiasis
http://en.wikipedia.org/wiki/File:Trypanosoma_sp._PHIL_613_lores.jpg
Sleeping Sickness
Symptoms:
Begins with fever, headaches, and joint pains.
Lymph nodes may swell enormously and parasite numbers
may be incredibly high. Greatly enlarged lymph nodes in
the back of the neck are tell-tale signs of the disease.
If untreated the parasite may cross the blood-brain barrier,
which causes the characteristic symptoms the disease is
named for. The patient becomes confused and the sleep
cycle is disturbed with the patient alternating between
manic periods and complete lethargy. Progressive mental
deterioration is followed by coma and death.
Sleeping Sickness
Trypanosome levels in infected patients show a
cycle of sharp peaks and valleys in parasite
numbers of approximately a week in length.
The cycle occurs because the immune system
recognizes the glycoprotein in the trypanosomes
coat and mounts an immune response to it,
which eliminates parasites with that glycoprotein.
Sleeping Sickness
Trypanosomes, however, possess about 1,000
different coat-building genes and periodically a
new one is turned on by a trypanosome that
produces a different coat, which the immune
system doesn’t recognize.
Trypanosomes with this new coat reproduce
undetected until the immune system can mount
a response to the new coat.
Sleeping Sickness
If the first generation of trypanosomes to infect a
host turned on their coat genes at random the
immune system could learn to recognize the
various possibilities quickly, remember them,
and eliminate the parasite.
Instead the coat-building genes are turned on in
pre-set sequence. This means that the immune
system every week or so is faced with a new
coat that it has not seen before.
Sleeping Sickness
As a result of the sequential coat-switching, the
immune system becomes chronically over-
stimulated and begins to attack the host’s body.
The overstimulation of the immune system and
the movement of parasites into the central
nervous, where they escape the immune system
altogether, eventually kills the patient.