Parasitism A Ecological niche and competition B Parasite

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 Ø i. e. all aspects of the organisms’ life Requirements Ø e. g. food type, food size, shelter, soil minerals Tolerances Ø e. g. temperature, humidity, soil p. H, 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? ØAll 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 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 Ø 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 Ø e. g. ticks, lice • An endoparasite lives within the host’s body Ø 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 Ø 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? Ø Ø 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 Ø e. g. indigenous Australian communities keep many dogs Ø high incidence of scabies lice infection • Also show high virulence due to low health of host Ø leads to ‘leather dog’

Life cycle stages increase transmission rates • Infected hosts are often incapacitated so cannot move parasite to new host Ø e. g. malaria and schistosomiasis • Increase transmission rate using … Ø vectors Ø waterborne dispersal stages

Parasites use host behaviour for transmission • Transmission is maximised by exploiting host behaviours Ø 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 Ø 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 movement sexual behaviour Mosquito and Plasmodium Frogs and flatworm Mayfly and nematode habitat choice anti-predator behaviour 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 Ø e. g. Sacculina spp. stop crab host from growing and reproducing Ø energy from host all directed to production of parasite Ø 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/PMC 1560305/#bib 9

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 Ø Sexual stages Ø Produce variation for evolution • Intermediate host = human Ø Needed for completion of parasite lifecycle Ø Developmental stage for getting to next host Ø Only asexual reproduction • Transmission? Ø By mosquito vector

Many parasites need more than one host species • Key example 2 - Schistosoma spp. • Platyhelminths that causes schistosomiasis • Definitive host = human Ø Sexual stages, produce variation for evolution • Intermediate host = water snail Ø Needed for completion of parasite lifecycle Ø Developmental stage for getting to next host Ø Only asexual reproduction • Transmission? Ø 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 Animal virus e. g. common cold Genetic material DNA or RNA Retrovirus e. g. HIV, influenza 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 Ø skin Ø nasal hairs e. g. chemical secretions Ø Ø 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 Ø group of about 1000 identical cells made from a common ancestor cell Ø 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 Ø each has different functions Ø 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! 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 Ø Neutralises action of parasite Ø Makes it easier for phagocytes to attack parasite Ø Quicker response if antigen is detected again Ø 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 to presented antigen Killer T cells receptors bind 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

Improvements due to better parasite control • 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 • So there is no way to study effects of treatments except using a host animal • e. g. Schistosoma parasite needs host signals to develop Vaccines are difficult to develop • Rapid antigen change has to be reflected in the design of vaccines • e. g. new influenza vaccine has to be made every year Host and parasite metabolism similarities • Difficult to find drug compounds that only target the parasite • 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: Ø water-borne stages e. g. schistosomiasis Ø 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 Ø e. g. in refugee camps Ø many hosts close together with poor sanitation Tropical climates allow parasites to spread rapidly Ø warmer so parasites can survive away from host Ø warmer so vectors reproduce quickly