Download AH2.5 Parasitism

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
AH Biology
Unit 2 – Organisms and Evolution
A: Ecological niche and competition
• Ecological niche = multidimensional summary
of requirements and tolerances of a species
Multidimensional
 i.e. all aspects of the
organisms’ life
Requirements
 e.g. food type, food size,
shelter, soil minerals
Tolerances
 e.g. temperature,
humidity, soil pH,
dissolved oxygen
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 overlap
• Effect on individuals of competition?
All have less resources so …
are less healthy and so …
have lower survival chances
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 niche
• A realised niche is occupied in
response to interspecific
competition
Niche of
Species 3
Niche of
Species 4
Niche of
Species 5
Niche of
Species 2
Fundamental
niche
Realised niche
of
of Species
Species 11
Example of fundamental and realised niches
Actual
adult
distribution
Competitive exclusion
Paramecium aurelia
Paramecium caudatum
• Occurs due to interspecific competition …
where the realised niches of the two species are very similar
• Called competitive exclusion because one species declines to local extinction
Resource partitioning
• Occurs due to interspecific competition …
where the realised niches of the two species are sufficiently different
• Potential competitors can co-exist by resource partitioning
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 available
• Disruptive selection and speciation
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 host
 How is this different from a
predator–prey relationship?
 Reproductive potential of parasite
is greater than that of the host
Ear mite releasing eggs
Ectoparasites and endoparasites
• An ectoparasite lives on the
surface of its host
 e.g. ticks, lice
• An endoparasite lives within the
host’s body
 e.g. tapeworm, Plasmodium
Many parasites are degenerate
• Host provides many of the parasite’s
needs so …
… evolution has favoured the loss of
non-useful structures and organs
• Parasites have become degenerate
 e.g. tapeworm lacks digestive system because
it absorbs digested food from animal’s
intestine
• This means that parasites have a narrow
niche in which they can survive and breed
Parasites tend to have a narrow niche
• Narrow niche also because parasites are very host specific
Parasite callus due to lice
Organisms involved in the parasite lifecycle
Definitive
host
An organism which plays an active role in the
transmission of the parasite (may also be a host)
Intermediate
host
Organism on which, or in which, the parasite
reaches sexual maturity
Vector
Organisms required for the parasite to complete
its life cycle (asexual stages of parasite life)
Malaria
Definitive host
(mosquito)
Intermediate host
(human)
Vector
(mosquito)
Schistosomiasis
Definitive host
(human)
Intermediate host
(water snail)
Vector
(none)
Why have asexual
and sexual phases?
• Asexual phase allows rapid
build-up of parasite population
• But no variation
• Sexual phase generates variation
so …
• allows rapid evolution
(Remember the Red Queen … )
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 virulence
• Traditional view is shown in the diagram …
… but it’s wrong!
• How would natural selection affect the virulence in each scenario?
Transmission and virulence go together
Virulence
X
• Low transmission
• Parasite selected to keep host active
enough to spread the parasite, so …
… means low virulence
• e.g. rhinovirus (common cold)
transmission relies on close contact, dies
off quickly in environment
Transmission
Transmission and virulence go together
• High transmission
• Parasite selected for maximum
reproduction as transmission will still
spread the parasite, so …
… means high virulence
• e.g. malaria, schistosomiasis, cholera
which have very effective transmission
mechanisms (more later!)
Virulence
Y
X
Transmission
• Hosts in a population do not have
equal parasite loads
• Why might this be?




variation in host health?
variation in host immune systems?
variation in host exposure to vectors?
variation in host behaviour?
Number of hosts with this parasite load
Distribution of parasites is not uniform
Number of parasites per host
Overcrowding of hosts increases transmission rate
• Hosts living at high density are closer
together so easier for parasite to spread
 e.g. indigenous Australian communities
keep many dogs
 high incidence of scabies lice infection
• Also show high virulence due to low
health of host
 leads to ‘leather dog’
Life cycle stages increase transmission rates
• Infected hosts are
often incapacitated
so cannot move
parasite to new host
 e.g. malaria and
schistosomiasis
• Increase transmission
rate using …
 vectors
 waterborne dispersal
stages
Parasites use host behaviour for transmission
• Transmission is maximised by exploiting host
behaviours
 e.g. schistosomiasis parasite released into water
so can infect humans as they wade in the water
• Host behaviour is often modified by parasites to
maximise transmission
 e.g. rabies virus makes a dog more aggressive so it
will bite and pass on virus in saliva
Examples of modified host behaviour
Modified host behaviour becomes part of the parasite’s extended phenotype
Host behaviour altered to increase the transmission rate.
Changes can alter the host’s:
foraging
behaviour
Mosquito and
Plasmodium
movement
sexual
behaviour
habitat
choice
anti-predator
behaviour
Frogs and
flatworm
Mayfly and
nematode
Ants and
flatworm
Rats and
Toxoplasma
Examples of modified host behaviour
Modified host behaviour becomes part of the parasite’s extended phenotype
Host behaviour altered to increase the transmission rate.
Changes can alter the host’s:
foraging
behaviour
movement
sexual
behaviour
habitat
choice
anti-predator
behaviour
Mosquito and
Plasmodium
Frogs and
flatworm
Mayfly and
nematode
Ant and
flatworm
Rats and
Toxoplasma
mosquito with
mature parasites
is more likely
to feed on blood from
more than one person
frogs develop
additional hind legs
so move slower
and are eaten by
predatory bird host
parasite 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
ant climbs
to top of blade of grass at
night instead of going to
nest so is eaten by
herbivore host
rat seeks out the smell
of cat urine
so are eaten by cat
and so parasite is ingested
by new host
Parasites modify host size and reproductive rate
• Benefits the parasite growth ,
reproduction or transmission
 e.g. Sacculina spp. stop crab host from
growing and reproducing
 energy from host all directed to production of
parasite
 host also treats parasite eggs as their own so
help to disperse them
Sacculina spp mimicking crab brood pouch
• Some parasites can suppress the host immune system
• Allows parasite to grow and reproduce more effectively
Mud snails - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1560305/#bib9
D: Parasitic life cycles
Common parasites include:
Protists
Arthropods
e.g. Plasmodium, amoeba
e.g. ticks, lice
Platyhelminths
Bacteria
e.g. Schistosoma, tapeworm
e.g. tuberculosis, syphilis
Nematodes
Viruses
e.g. threadworm, elephantiasis
e.g. influenza, HIV
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)
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)
e.g. tick
e.g. tapeworm species
e.g. Plasmodium
Direct contact
Parasite transfers on to
outside of a new host
Consumption of
intermediate host
Often transmitted
by vectors
New host ingests eggs from
New host ingests tapeworm
environment
cysts in flesh
Mosquito passes parasite to
new host
Direct contact
Some parasites need only one host species
 Whole life cycle can be completed within one host
 Direct contact used as method of transmission
 e.g. ectoparasitic arthropods
 e.g. endoparasitic amoebas
Entamoeba hystolytica
which causes amoebic dysentery
Many parasites need more
than one host species
• Key example 1 – Plasmodium spp.
• Protists that cause malaria
• Definitive host = mosquito
 Sexual stages
 Produce variation for evolution
• Intermediate host = human



Needed for completion of parasite lifecycle
Developmental stage for getting to next host
Only asexual reproduction
• Transmission?
 By mosquito vector
Many parasites need more
than one host species
• Key example 2 - Schistosoma spp.
• Platyhelminths that causes schistosomiasis
• Definitive host = human
 Sexual stages, produce variation for evolution
• Intermediate host = water snail



Needed for completion of parasite lifecycle
Developmental stage for getting to next host
Only asexual reproduction
• Transmission?

By waterborne stages (no vector)
Bacteria and viruses need only one host species
 Microparasites with their whole life cycle completed in one host
Caused by
bacterium
Infects all parts
of body, most
commonly
lungs
Transmitted in
aerosol from
coughs or in
unpasteurised milk
Influenza
Caused by
virus
Infects joints,
muscles and
respiratory
tract
Transmitted in
aerosol from
coughs and sneezes
HIV / AIDS
Caused by
virus
Infects T helper
lymphocytes of
immune system
Transmitted in
blood or by sexual
contact
Tuberculosis
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
Retrovirus e.g. HIV, influenza
Animal virus e.g. common cold
Genetic material
DNA or RNA
Packaged in protective
protein coat
Many have a membrane envelope
 Outer surface has antigens which the virus uses to attach to a host cell
 Antigens can sometimes be detected by host immune system
DNA virus replication
5. Virus particles are
assembled and burst
out of host cell
1. Virus antigens attach to
host cell surface
2. Virus DNA
genome
inserted into
the host cell
4. Virus genes are transcribed
to RNA and translated to
make viral proteins
3. Virus DNA is replicated by
host enzymes
Retrovirus replication changes RNA into DNA
1. Virus antigens
attach to host
cell surface
2. Virus RNA
genome inserted
into the host cell
Viral enzyme called reverse transcriptase
reads viral RNA to form DNA
5. Virus particles are
assembled and burst
out of host cell
4. Virus genes are
transcribed to RNA
and translated to
make viral proteins
New formed viral DNA is inserted
into the genome of host cell
E: Immune response to parasites by mammals
Mammal
body fluids
First line
Stop the parasite
from entering body
Second line
Attack parasite for
being foreign
Third line
Attack specific
antigens on parasite
Non-specific
Parasite
outside
defences
the host
Non-specific
response
Parasite
has got past
Specific cellular
defences
Parasite
has evaded
the first line defences
second line defences
Physical barriers
Chemical secretions
Natural killer cells
Inflammation
Phagocytes
Lymphocytes
Antibodies
Non-specific defences
First line tries to stop the parasite from getting in
e.g. physical barriers
 skin
 nasal hairs
e.g. chemical secretions




mucus in nose and lungs
ear wax
tears with anti-bacterial chemicals
acid secretions on skin and in stomach
Non-specific responses
Defences for when the parasite has entered body fluids
inflammatory
response
phagocytes
engulfing
foreign cells
natural killer
cells destroying
abnormal cells
• histamine release causes blood vessels to dilate
• blood vessels more permeable so fluid leaks into tissue
• tissue swells up so other cells can easily access area
• cells with foreign antigens are engulfed
• phagocyte digests cell
• phagocyte presents foreign antigens on surface (important!)
• cells infected by virus have foreign proteins on surface
• natural killer cells release chemical signals
• infected cells induced to kill themselves (apoptosis)
Specific cellular defences
1. Lymphocytes
 White blood cells found mainly in lymph glands
 Each lymphocyte is part of a clone
 group of about 1000 identical cells made from a
common ancestor cell
 each ancestral cell is committed to make just one
type of receptor protein
 So each lymphocyte has just one type of
receptor protein on surface
 Receptor protein binds to a specific antigen
(Each person can make about a billion different types of receptor protein)
Specific cellular defences
2. Immune surveillance
 Lymphocytes check the lymph fluid for antigens
 Lymphocyte only activated if its receptor binds to its antigen
 Three types of lymphocytes
 each has different functions
 each activated in a different way
killer
Specific cellular defences
3. Clonal selection of B and T lymphocytes
• After lymphocyte binds to antigen, it divides and increases in number
• Called clonal selection
Receptors on
B lymphocyte clones bind
to specific antigen
Phagocytes present
antigens to
T helper lymphocyte clones
Phagocytes present
antigens to
T killer lymphocyte clones
This one fits!
B lymphocytes divide and
rapidly increase in number
T helper lymphocytes target
immune response cells and
activate them
T lymphocytes divide and
rapidly increase in number
Specific cellular defences
4. Action of lymphocytes
Goodbye,
sucker!
I remember
you!
I remember
you!
I remember
you!
I remember
you!
I remember
you!
I remember
you!
B lymphocyte clones
produce specific antibodies
(same shape as their receptors)
T killer lymphocyte clones
destroy infected cells
by inducing apoptosis
Long term survival of
some members of
B and T lymphocyte clones
Antibodies bind to antigens
Activates ‘cell death’ signals
within the infected cell
Immunological memory


Neutralises action of parasite
Makes it easier for
phagocytes to attack parasite
 Quicker response if antigen is
detected again
 Basis of vaccinations
Sneeze attack ̶ the influenza virus just got you!


Mucus barrier in nose and lungs
didn’t fully work
Phagocytes got a few viruses
but most got in to infect cells
B cell receptors bind to
antigen
Virus with antigen
Engulfed by phagocyte which
presents antigens on surface
activate Helper
T cells receptors bind activate Killer T cells receptors bind
to presented antigen
to presented antigen
B cells divide and increase in
number
T killer cells divide and
increase in number
B cells produce specific
antibodies
T killer cells cause apoptosis
of infected cells
Lymphocytes kept as
immunological memory
Parasites v. immune system
Endoparasites have evolved strategies
to resist the immune system
1. Mimic host cell
antigens
• Evades detection by
immune system
3. Antigenic variation in subsequent
generations
• Evolve faster than immune system
can respond to new antigens
2. Modify the host’s
immune response
• Reduce chances of
destruction
F: Challenges in treatment and control
 Epidemiology – study of the outbreak and spread of infectious disease
 Vaccinations reduce the spread of disease
 Enough people vaccinated can bring herd immunity
F: Challenges in treatment and control
 Epidemiology – study of the outbreak and spread of infectious disease
 Vaccinations reduce the spread of disease
 Enough people vaccinated can bring herd immunity
F: Challenges in treatment and control
 Epidemiology – study of the outbreak and spread of infectious disease
 Vaccinations reduce the spread of disease
 Enough people vaccinated can bring herd immunity
Herd immunity threshold
Density of resistant hosts needed in the population to prevent an epidemic
• Reduced child mortality
• Population-wide improvements in child development and intelligence …
… because individuals have more resources for growth and development
Difficulties in developing anti-parasite medicines
Some parasites are
difficult to culture in the
laboratory
Vaccines are difficult to
develop
Host and parasite
metabolism similarities
• So there is no way to
study effects of
treatments except
using a host animal
• Rapid antigen change
has to be reflected in
the design of vaccines
• Difficult to find drug
compounds that only
target the parasite
• e.g. Schistosoma
parasite needs host
signals to develop
• e.g. new influenza
vaccine has to be
made every year
• e.g. chloramphenicol
blocks bacterial
ribosome … and
mitochondrial
ribosome
Attacking other parts of the parasite lifecycle
 Often these may be the only practical control strategies
 Medicines are too difficult (or costly?) to develop
Many parasites spread by:
 water-borne stages e.g. schistosomiasis
 vectors e.g. malaria
Coordinated vector
control
Reduce vector populations
and prevent vectors from
infecting new host
Civil engineering
projects to improve
sanitation
Parasites not
transferred from human
waste into drinking or
bathing water
Parasites spread most rapidly
where control is difficult
 Overcrowding allows parasites to spread
rapidly
 e.g. in refugee camps
 many hosts close together with poor sanitation
 Tropical climates allow parasites to spread
rapidly
 warmer so parasites can survive away from host
 warmer so vectors reproduce quickly