AH Biology Unit 2 – Organisms and Evolution - PowerPoint Presentation

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AH Biology

Unit 2 – Organisms and Evolution

Parasitism

A: Ecological niche and competition

B: Parasite niches C: Transmission and host behaviour D: Parasitic life cycles E: Immune response to parasites F: Challenges in treatment and control

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A: Ecological niche and competition

Ecological niche =

multidimensional

summary of requirements and tolerances of a speciesMultidimensionali.e. all aspects of the organisms’ life

R

equirementse.g. food type, food size, shelter, soil minerals

Tolerances

e.g. temperature, humidity, soil pH, dissolved oxygen

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Niche overlap leads to competition

Niche overlap occurs when …

... different species have similar resource requirements and tolerances

Most intense competition where there is most niche overlapEffect on individuals of competition?

All have less resources so …are less healthy and so …have lower survival chances

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Niches can be changed by competition

A species has a

fundamental niche

that it occupies in the absence of interspecific competition

Interspecific competition can reduce the range of this nicheA realised niche is occupied in response to interspecific competitionFundamental nicheof Species 1Niche of Species 2Niche of Species 3Niche of Species 4

Niche of

Species 5Realised nicheof Species 1

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Example of fundamental and realised

niches

Actual adult distribution

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Competitive exclusion

Occurs due to

interspecific

competition …

where the realised niches of the two species are very similarCalled competitive exclusion because one species declines to local extinctionParamecium aurelia

Paramecium

caudatum

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Resource partitioning

Occurs due to interspecific competition …

where the realised niches of the two species

are

sufficiently differentPotential competitors can co-exist by resource partitioning

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Natural selection leads to resource partitioning

Natural selection works on competing organisms in same area

Selection favours specialisation

on

obtaining different aspects of the resources availableDisruptive selection and speciation

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B: Parasite niches

A parasite is a symbiont that gains benefit in terms of nutrients at the expense of its host

e

.g.

ear mite feeds on blood of mammal hostHow is this different from a predator–prey relationship?Reproductive potential of parasite is greater than that of the hostEar mite releasing eggs

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Ectoparasites and endoparasites

An

ectoparasite

lives on the surface of its

hoste.g. ticks, liceAn endoparasite lives within the host’s bodye.g. tapeworm, Plasmodium

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Many parasites are degenerate

H

ost provides many of the parasite’s needs so …

… e

volution has favoured the loss of non-useful structures and organsParasites have become degeneratee.g. tapeworm lacks digestive system because it absorbs digested food from animal’s intestineThis means that parasites have a narrow niche in which they can survive and breed

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Parasites tend to have a narrow niche

Narrow niche also because parasites are very host specific

Parasite callus due to lice

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Organisms involved in the parasite lifecycle

An organism which plays an active role in the transmission of the parasite (may also be a host

)

O

rganism on which, or in which, the parasite reaches sexual maturity Organisms required for the parasite to complete its life cycle (asexual stages of parasite life)Definitive hostIntermediate hostVector

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D

efinitive host

Intermediate host

V

ector

(mosquito)

(

human

)

(mosquito)

Malaria

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(human)

(water snail)

(none)

D

efinitive host

Intermediate host

V

ector

Schistosomiasis

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Why have asexual and sexual phases?

Asexual phase allows rapid

build-up of parasite

population

But no variationSexual phase generates variation so …allows rapid evolution (Remember the Red Queen … )

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C: Transmission and host behaviour

Spread

of a parasite to a host is called

transmission

Harm caused to a host species by a parasite is called virulenceTraditional view is shown in the diagram …… but it’s wrong!How would natural selection affect the virulence in each scenario?

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Transmission and virulence go together

Low transmissionParasite selected to keep host active enough to spread the parasite, so …

… means low virulencee.g. rhinovirus (common cold) transmission relies on close contact, dies off quickly in environment

Transmission

VirulenceX

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Transmission and virulence go together

High transmission

Parasite selected for maximum reproduction as transmission will still spread the parasite, so …

… means high virulencee.g. malaria, schistosomiasis, cholera which have very effective transmission mechanisms (more later!)

TransmissionVirulenceXY

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Distribution of parasites is not uniform

Hosts in a population do not have equal parasite loads

Why might this be?

v

ariation in host health?variation in host immune systems?variation in host exposure to vectors?variation in host behaviour?Number of parasites per host

Number of hosts with this parasite load

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Overcrowding of hosts increases transmission rate

H

osts living at high density are c

loser together so easier for parasite to spread

e.g. indigenous Australian communities keep many dogshigh incidence of scabies lice infectionAlso show high virulence due to low health of hostleads to ‘leather dog’

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Life cycle stages increase transmission rates

I

nfected hosts are often incapacitated so cannot move parasite to new host

e.g. malaria and

schistosomiasisIncrease transmission rate using …vectorswaterborne dispersal stages

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Parasites use host behaviour for transmission

Transmission is maximised by

exploiting

host behaviourse.g. schistosomiasis parasite released into water so can infect humans as they wade in the waterHost behaviour is often modified by parasites to maximise transmissione.g. rabies virus makes a dog more aggressive so it will bite and pass on virus in saliva

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Examples of modified host behaviour

Modified host behaviour becomes part of the parasite’s

extended phenotype

H

ost behaviour altered to increase the transmission rate.Changes can alter the host’s

:

foraging behaviour

movement

sexual behaviour

h

abitat choice

a

nti-predator behaviour

Mosquito and Plasmodium

Mayfly and

nematode

Ants and

flatworm

Rats and

Toxoplasma

Frogs and

flatworm

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Examples of modified host behaviour

Modified host behaviour becomes part of the parasite’s

extended phenotype

foraging behaviour

movementsexual behaviour

h

abitat choice

anti-predator behaviour

Mosquito and Plasmodium

Mayfly andnematode

Ant and

flatworm

Rats and

Toxoplasma

Frogs and

flatworm

rat seeks out the smell

of cat urine

so are eaten by cat

and so parasite is ingested by new host

frogs develop

additional hind legs

so move slower

and are eaten by

predatory bird host

ant climbs

to top of blade of grass at night instead of going to nest so is eaten by herbivore host

mosquito with

mature parasites

is more likely

to feed on blood from

more than one person

p

arasite has to return to water so mayfly females go to lay eggs even if none present; males behave like females and go to lay eggs

H

ost

behaviour

altered to increase the transmission rate.

C

hanges can alter the

host’s

:

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Parasites modify host size and reproductive rate

B

enefits the parasite growth , reproduction or transmission

e.g.

Sacculina spp. stop crab host from growing and reproducingenergy from host all directed to production of parasitehost also treats parasite eggs as their own so help to disperse themSacculina spp mimicking crab brood pouch

Some parasites can suppress

the host immune system

Allows parasite to grow and reproduce more effectivelyMud snails - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1560305/#bib9

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D: Parasitic life cycles

Common parasites include:

And … annelids (e.g. leech), fungi (e.g. athlete’s foot), angiosperms (e.g. bird’s nest orchid), mammals (e.g. vampire bat), fish (e.g. lamprey)

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Often transmitted

by

vectors

Mosquito passes parasite to new host

e.g. PlasmodiumConsumption of intermediate hostNew host ingests tapeworm cysts in fleshDirect contactNew host ingests eggs from environment

e.g. tapeworm species

Direct contact

Parasite transfers on to outside of a new host

e.g. tick

Different methods of transmission are used

Method depends on where the parasite will live in the host

Ectoparasites

Endoparasites

of body

cavities

(such

as guts

)

Endoparasites

of body

tissue

(such

as blood

)

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Some parasites need only one host species

Whole life cycle can be

completed within one host

Direct contact used as method of

transmissione.g. endoparasitic amoebase.g. ectoparasitic arthropods

Entamoeba hystolytica

which causes amoebic dysentery

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Many parasites need more than one host species

Key example 1 –

Plasmodium

spp.Protists that cause malaria

Definitive host = mosquitoSexual stagesProduce variation for evolutionIntermediate host = humanNeeded for completion of parasite lifecycleDevelopmental stage for getting to next hostOnly asexual reproductionTransmission?By mosquito vector

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Key example 2 -

Schistosoma

spp.

Platyhelminths that causes schistosomiasis

Definitive host = humanSexual stages, produce variation for evolutionIntermediate host = water snailNeeded for completion of parasite lifecycleDevelopmental stage for getting to next hostOnly asexual reproductionTransmission?By waterborne stages (no vector)Many parasites need more than one host species

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Bacteria and viruses need only one

host species

Microparasites

with their whole life cycle

completed in one host

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Viruses can only replicate inside a host cell

Bacteria can replicate if they are supplied with the correct conditions

Viruses are infectious agents that can only replicate inside a host cell

Genetic material

DNA or RNA Packaged in protectiveprotein coatMany have a membrane envelope

Animal virus e.g. common cold

Retrovirus e.g. HIV, influenza

O

uter surface has

antigens

which the virus uses to

attach to a host cell

A

ntigens

can sometimes

be detected

by host immune system

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DNA virus replication

Virus antigens attach to host cell surface

Virus

DNA is replicated by host enzymes

Virus DNA genome inserted into the host cellVirus genes are transcribed to RNA and translated to make viral proteins

Virus particles are assembled and burst out of host cell

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Retrovirus replication changes RNA into DNA

Virus antigens attach to host cell surface

Virus

RNA

genome inserted into the host cellViral enzyme called reverse transcriptase reads viral RNA to form DNANew formed viral DNA is inserted into the genome of host cell

Virus genes are transcribed to RNA and translated to make viral proteins

Virus

particles are assembled and burst out of host cell

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Mammal

body fluids

Parasite has evaded second line defences

Parasite has got past the first line defences

Third lineAttack specific antigens on parasiteSpecific cellular defencesLymphocytesAntibodiesParasite outside the hostE: Immune response to parasites by mammals

Second

lineAttack parasite for being foreign

Non-specific responseNatural killer cellsInflammationPhagocytes

First line

Stop the parasite

from entering body

Non-specific defences

Physical barriers

Chemical secretions

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Non-specific defences

First line tries to stop the parasite from getting in

e.g.

p

hysical barriersskinnasal hairs e.g. chemical secretionsmucus in nose and lungsear waxtears with anti-bacterial chemicals

acid secretions on skin and in stomach

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Non-specific

responses

Defences for when the parasite

has entered body

fluids

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Specific cellular defences1. Lymphocytes

White blood cells found mainly in

lymph

glands

Each lymphocyte is part of a clonegroup of about 1000 identical cells made from a common ancestor celleach ancestral cell is committed to make just one type of receptor proteinSo each lymphocyte has just one type of receptor protein on surfaceReceptor protein binds to a specific antigen

(Each person can make about a

billion different types of receptor protein)

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killer

Specific cellular defences

2. Immune surveillance

Lymphocytes check the lymph fluid for antigens

Lymphocyte only activated if its receptor binds to its antigenThree types of lymphocyteseach has different functionseach activated in a different way

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This one fits!

Specific cellular defences

3. Clonal selection of B and T lymphocytes

Receptors on

B lymphocyte clones bindto specific antigenPhagocytes present antigens to T killer lymphocyte clonesPhagocytes present antigens to T helper lymphocyte clonesB lymphocytes divide and rapidly increase in numberT helper lymphocytes target immune response cells and activate them

T lymphocytes divide and rapidly increase in number

After lymphocyte binds to antigen, it divides and increases in numberCalled

clonal selection

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Specific cellular defences4. Action of lymphocytes

B lymphocyte clones

produce specific antibodies (same shape as their receptors)

T killer lymphocyte clones destroy infected cells

by inducing apoptosisLong term survival ofsome members of B and T lymphocyte clonesGoodbye, sucker!I remember you!I remember you!I remember you!

Antibodies bind to antigensNeutralises action of parasiteMakes it easier for phagocytes to attack parasite

Activates ‘cell death’ signals within the infected cellI

mmunological memoryQuicker response if antigen is detected againBasis of vaccinations

I remember you!

I remember you!

I remember you!

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Lymphocytes kept as immunological memory

Sneeze attack

Mucus barrier in nose and lungs didn’t fully work

Phagocytes got a few viruses but most got in to infect cells

̶ the influenza virus just got you!

Engulfed by phagocyte which presents antigens on surface

B cell receptors bind to antigen

Helper T cells receptors bind to presented antigen

B cells divide and increase in number

Virus with antigen

Killer T cells receptors bind to presented antigen

T killer cells divide and increase in number

T killer cells cause apoptosis of infected cells

B cells produce specific antibodies

activate

activate

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Parasites v. immune system

Mimic host

cell antigens

Evades

detection by immune systemModify the host’s immune responseReduce chances of destruction

Antigenic variation in subsequent generations

Evolve faster than immune

system can respond to new antigens

Endoparasites

have evolved strategies

to resist

the immune

system

Slide47

F: Challenges in treatment and control

Epidemiology

– study

of the outbreak and spread of infectious

diseaseVaccinations reduce the spread of diseaseEnough people vaccinated can bring herd immunity

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F: Challenges in treatment and control

Epidemiology

– study

of the outbreak and spread of infectious

diseaseVaccinations reduce the spread of diseaseEnough people vaccinated can bring herd immunity

Slide49

F: Challenges in treatment and control

Epidemiology

– study

of the outbreak and spread of infectious

diseaseVaccinations reduce the spread of diseaseEnough people vaccinated can bring herd immunityHerd immunity thresholdDensity of resistant hosts needed in

the population to prevent an epidemic

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Improvements due to better parasite control

R

educed

child

mortalityPopulation-wide improvements in child development and intelligence … … because individuals have more resources for growth and development

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Difficulties in developing anti-parasite medicines

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Reduce vector populations and prevent vectors from infecting new host

Coordinated

vector control

Parasites not transferred from human waste into drinking or bathing water

Civil engineering projects to improve sanitation

Attacking other parts of the parasite lifecycle

Often these may be the only practical control

strategiesMedicines are too difficult (or costly?) to develop

Many parasites spread

by:water-borne stages e.g.

schistosomiasis

vectors

e.g.

malaria

Slide54

P

arasites

spread most

rapidly where control is difficult

Overcrowding allows parasites to spread rapidlye.g. in refugee campsmany hosts close together with poor sanitationTropical climates allow parasites to spread rapidlywarmer so parasites can survive

away from host

warmer so vectors reproduce quickly

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