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 (see pages 90-92 of text).

Protozoans

Eukaryotic cell was developed through endosymbiosis. In distant past aerobic bacteria appear to have been engulfed by anaerobic bacteria, but not digested. Ultimately developed symbiotic relationship with engulfed aerobic bacteria becoming mitochondria and eukaryotes 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.
can be asexual by fission or budding or sexual by conjugation or syngamy (fusion of gametes).

Reproduction

Protozoans
The

protozoa were once considered a single phylum, now at least 7 phyla are recognized. also once grouped with unicellular algae into the Protista an even larger paraphyletic group.

Were

Movement in Protozoa
Protozoa

move mainly using cilia or flagella and by using pseudopodia also used for feeding in many small metazoans.

Cilia

Cilia and flagella

No

real morphological distinction between the two structures although cilia are usually shorter and more abundant and flagella fewer and longer. flagellum or cilium is composed of 9 pairs of longitudinal microtubules arranged in a circle around a central pair.

Each

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 organisms cell membrane. anchors where it inserts into the main body of the cell with a basal body.

Axoneme

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

Oddly,

the humble flagellum has been 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 schools is the idea of Intelligent Design.

Latest

Flagella, intelligent design and irreducible complexity

The concept of intelligent design is outlined most clearly in Michael Behes book Darwins 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

If

structures 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 Behes 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 that cilia could not have evolved in a step-by step process of gradual improvement.

Flagella, intelligent design and irreducible complexity

Since the publication of Behes book, it has been demonstrated repeatedly that things he has claimed to be irreducibly complex are not in fact so. 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.

Movement in Protozoa: Pseudopodia

Pseudopodia

are chief means of locomotion of amebas but are also formed by other protozoa and ameboid cells of many invertebrates. ameboid movement the organism extends a pseudopodium in the direction it wishes to travel and then flows into it.

In

Pseudopodia

Ameboid 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 amebas involves using pseudpodia to surround and engulf a particle in the process of phagocytosis.

The

particle 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. some ciliates budding occurs in which a smaller progeny cell is budded off which later grows to adult size.

In

Binary fission in various taxa

Sexual reproduction in protozoa

All

protozoa reproduce asexually, but sex is widespread in the protozoa too. ciliates such as Paramecium a type of sexual reproduction called conjugation takes place in which two Paramecia join together and exchange genetic material

In

Figure 11.28

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
In

1897 an equally important discovery, the mode of transmission of malaria, was discovered by Ronald Ross. identification of the Anopheles mosquito as the transmitting agent earned him the 1902 Nobel Prize and a knighthood in 1911.

His

Plasmodium
There

are four species of Plasmodium: P. falciparum, P. vivax, P.ovale and P. malariae. falciparum causes severe often fatal malaria and is responsible for most deaths, with most victims being children.

P.

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

Plasmodium

has two hosts: mosquitoes and humans. reproduction takes place in the mosquito and the parasite is transmitted to humans when the mosquito takes a blood meal

Sexual

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 mosquitos stomach to produce zygotes. These zygotes develop into motile elongated ookinites. The ookinites invade the mosquitos 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

The

Plasmodium parasite engages in a number of manipulative behaviors to enhance its chances of being transmitted between hosts. manipulations are a common feature of parasite behavior in general as we will see throughout the semester.

Such

How Plasmodium enhances transmission rates

Mosquitoes

risk death when feeding and attempt to minimize risk and maximize reward when doing so. obtain blood a mosquito must insert its proboscis through the skin and then locate a blood vessel. The longer this takes, the greater the risk.

To

How Plasmodium enhances transmission rates

As

soon as the mosquito hits a blood vessel the hosts body responds by clotting the wound. clump around the proboscis and release chemicals which cause the platelets to clot together.

Platelets

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 parasites 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.

In

the salivary gland the parasite cuts off the mosquitos 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. a result, the parasite is spread more widely.

As

Behavior of Plasmodium in humans

Plasmodium enters the blood steam through a mosquito bite. The parasite must avoid the hosts 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

The

immune 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

The

parasites leave the liver, reenter the bloodstream, and find a red blood cell to enter. parasite spends two days in a red blood cell consuming the hemoglobin and reproducing.

Each

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 cells 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. 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

Old

red blood cells eventually lose their elasticity and become stiff. that show signs of such aging are filtered out as they pass through the spleen and destroyed.

Those

Behavior of Plasmodium in humans

Plasmodium

cannot swim but uses hooks to move along the blood vessels. the parasites tip are sensors that respond only to young red blood cells and clasp on to proteins on the cells surface.

At

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 cells membrane to open and let the parasite squeeze in. takes only about 15 seconds for the parasite to get in.

It

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. toxic core of the hemoglobin molecule is processed into an inert molecule called hemozoin.

The

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 cells springiness for as long as possible so it 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. latch proteins however do stimulate the immune system.

The

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. each generation some of the new parasites switch on a new latch gene and so the immune system is always playing catch up.

In

Effects of malaria on human evolution

The

intense selection pressure imposed by malaria has resulted in a large number of mutations that provide protection against the parasite being selected for in humans. best known is sickle cell anemia.

The

Anti-malaria mutations: Sickle cell anemia

Sickle

cell anemia is a condition common in West Africans (and African Americans of West African ancestry). sickle cell anemia red blood cells are sickle shaped as a result of a mutation which causes hemoglobin chains to stick together.

In

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. a result the geographic distribution of the allele and malaria in Africa match quite closely.

As

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. with G6PD-202A a reduced activity variant common in Africa have a significantly reduced risk of suffering severe malaria.

People

Anti-malaria mutations: Thalassemia

Thalassemia:

People with thalassemia make the ingredients of hemoglobin in the wrong amounts. many or too few or hemoglobin chains are produced and when they are assembled into hemoglobin molecules spare chains are left over.

Too

Other anti-malaria mutations: Thalassemia

Extra chains clump together and cause major problems in the cell. These clumps grab oxygen, but dont 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 cant slip through capillaries. The rigid cell walls make it hard for the parasite to enter the cell and the cells rigidity appears to prevent the parasite pumping in phosphates and sulphates it needs to survive.

Anti-malaria mutations:

One major advantage of these various antimalarial mutations appears to that they provide a natural vaccination program for children. By slowing the development of the parasite these mutations give a childs nave immune system time to overcome Plasmodiums 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.

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