Unit 2 - Parasitism Flashcards
Ecological niche
All the factors that influence the distribution of an individual species.
Includes abiotic factors (eg. temperature, pH, salinity) and biotic interactions (eg. parasites and predator-prey).
It summarises the tolerances and requirements of a species.
Fundamental niche
The set of resources that a species is capable of using in the absence of interspecific competition.
Realised niche
The set of resources that a species actually uses in response to the presence of interspecific competition.
Competitive exclusion principle
Occurs as a result of interspecific competition when the realised niches of 2 species are almost identical.
One species will decline resulting in local extinction. eg. grey/red squirrels
Resource partitioning
2 species living in a habitat have similar requirements, but can co-exist due to different realised niches.
2 species exploit different components of the resource, reducing competition. eg different beak lengths in wading birds.
Parasitism
A type of symbiosis where the parasite gains nutrients at the expense of the host.
These resources are used for growth and reproduction, and the host also uses resources to defend itself against parasite attack.
The reproductive potential of the parasite is much greater that that of the host.
Ectoparasite
Live and feed on the surface of their host eg. ticks, lice
Endoparasite
Live within their host eg. tapeworm, Plasmodium (malaria)
Parasite niche
As a result of co-evolution, parasite adaptations are selected in response to adaptations that have evolved in the host. (Red Queen hypothesis).
Parasites tend to have a narrow, specialised niche as a result.
They are host specific and show resource partitioning - different species inhabiting different parts of the host’s body.
Parasites are often degenerate - they lack structures found in other organisms, eg. a digestive system, sense organs.
Symbiosis
An intimate ecological relationship between 2 species.
Parasitism = +/- relationship
Mutualism = +/+
Commensalism = +/o
Direct lifecycle
Lifecycle is completed within one species.
Often use direct contact as a transmission mechanism.
Often ectoparasites eg. headlice
Indirect lifecycle
The parasite requires more than one host to complete its lifecycle.
Definitive host - the organism in which the parasite carries out sexual reproduction.
Intermediate host - the organism in which developmental/asexual stages occur.
Vectors - play an active part in the transmission of the parasite and increase efficiency of transmission. May also (but not always) be a host eg. mosquito
Plasmodium
Protists that cause malaria in humans.
An infected mosquito acting as a vector, bites a human and transmits the parasite.
The parasites reproduce asexually in the liver and red blood cells, which burst releasing gametocytes.
These are collected by another mosquito, mature into gametes and sexual reproduction occurs in the mosquito (definitive host).
The parasites migrate to the salivary glands of the mosquito, ready to infect the next host.
Schistosoma
Platyhelminthes that cause Schistosomiasis in humans.
Larvae burrow through the skin of humans, as they wade in fresh water.
They migrate to the small intestine and carry out sexual reproduction.
Fertilised eggs pass out in the faeces into the water.
The eggs hatch and form larvae that infect water snails.
Asexual reproduction in the snail produces a motile larva that can swim and burrow into human skin.
Virus
An infectious parasitic agent that can only replicate inside a host cell.
They are not really ‘living’ as they don’t carry out any normal functions of living organisms except reproduction, which requires a host cell.
Virus structure
Viruses are made of nucleic acid (DNA or RNA) packaged in a protective protein coat (capsid).
The outer surface has antigens (proteins) coded for by viral genes.
Antigens may trigger an immune response in the host organism, if they are recognised as ‘foreign’.
DNA viruses
Their genetic material is in the form of DNA. eg. smallpox, herpes.
Virus antigens ‘dock’ with receptors on the surface of the host cell, and the host cell is infected with viral DNA.
The virus genome is replicated by the host cell, and viral genes are transcribed to RNA, which is translated into viral proteins.
New virus particles are assembled and are released from the host cell, ready to infect other cells.
RNA viruses
Have an RNA genome, eg. influenza, hepatitis C
Reproduce as DNA viruses, except the viral genome is replicated directly using an enzyme from the virus.
Viral DNA is never made.
RNA retroviruses
Use the enzyme reverse transcriptase to make a DNA copy of the viral genome. eg. HIV
The DNA copy is inserted into the genome of the host cell, and is replicated as part of the normal cell cycle in the host.
Viral genes are then expressed to form new virus components, which are assembled and burst out of the host cell.
Transmission
The spread of a parasite to a new host.
Virulence
The harm that a parasite causes a host species, which reduces its evolutionary fitness.
Increasing parasite transmission rates
- Overcrowding of hosts, living at high population densities. eg. head lice. spread by direct contact.
- Vectors allow the parasite to spread even if the host is incapacitated, eg. by malaria
- Waterborne dispersal allows parasites to enter the water and spread to new hosts, if the original host is immobilised and improves transmission efficiency.
Factors that increase virulence
High transmission rates exert a selection pressure for increased virulence, to increase parasite growth and reproduction.
- suppress the host’s immune system so parasites are not attacked.
- modify the size of the host - make it grow bigger so it can support more parasites.
- reduce the host’s reproduction rate so resources are directed to parasite reproduction.
Modification/exploitation of host behaviour
Used to maximise chances of transmission.
Schistosoma exploits the wading behaviour of mammals.
If the host’s behaviour is modified it becomes part of the extended phenotype of the parasite. eg. habitat choice - an ant infested with parasitic flatworms will climb up a blade of grass to rest, and is more likely to be eaten by a sheep.
First line defences
Non- specific physical and chemical barriers that prevent parasites from entering the body fluids.
Physical - epithelial tissue, nasal hairs.
Chemical - mucus (moved by cilia), stomach acid, sweat, hydrolytic enzymes in tears.
Second line defences
Non- specific responses that happen after the parasite enters the body.
The 3 types are:
- inflammatory response
- phagocytes
- natural killer cells
Inflammatory response
Injured or infected cells release histamine (a signalling molecule).
Causes blood vessels to dilate, increasing blood flow so the area becomes red and warm.
Blood vessels become more permeable and fluid leaks into the tissues causing swelling and pain.
Anti-microbial proteins and phagocytes migrate to the area.
Phagocytes
White blood cells that migrate from blood to tissue fluid.
They engulf and digest foreign objects that lack ‘self’ antigens using powerful enzymes found in lysosomes.
Dead phagocytes leave infected wounds as pus.
Natural killer cells
Another type of white blood cell that can migrate from the blood into the tissues.
Detect abnormal cell surface proteins on virus infected and cancerous cells.
Killer cells attach to the infected cell and release chemicals into it, triggering apoptosis.
Phagocytes engulf and digest remaining debris.
Third line defences
Specific responses triggered by antigens on the surface of the parasite.
Involve specific lymphocytes.
Cytokines
Chemicals released by damaged or invaded tissues.
Increase blood flow so that non-specific and specific white blood cells, which are constantly circulating, gather at the site of infection.
Lymphocytes
White blood cells found mainly in lymph glands.
Have one type of antigen-receptor protein on their surface, which can bind to one specific antigen.
Immune surveillance
Carried out by lymphocytes in the lymph glands as lymph (tissue fluid drained from the cells) passes through.
The lymphocytes check for specific antigens, using the receptor proteins on their surface.
Phagocytes are also checked for presented antigen fragments.
Clonal selection
A specific lymphocyte binds to a target antigen and is activated.
It divides rapidly to make many identical clones, with the same specific antigen receptor.
Antibodies
Globular proteins released by a certain type of lymphocyte, which are specific for a target antigen on a parasite.
The antibodies bind to the parasite, forming an antibody-antigen complex, which immobilises the parasite or triggers its cells to undergo lysis.
The complex can also be engulfed by a phagocyte.
Killer lymphocytes
Specific lymphocytes that bind to cells infected with parasites and induce apoptosis by injecting chemicals.
Immunological memory
Some lymphocyte clones remain as memory cells, once the infection has been defeated.
If a specific antigen is detected again, the response is larger and faster.
Produced as a result of vaccination - a harmless version of the parasite is presented to the immune system, to trigger an immune response and to produce memory cells.
Immune evasion
Parasites have evolved ways to evade the host’s immune system, as a result of the ongoing ‘Red Queen’ race between host and parasite.
- mimic host antigens to hide from the immune system, eg. Schistosoma
- antigenic variation resulting in constantly changing cell surface antigens eg. Plasmodium
- integrate parasite genome into host genome, remaining in an inactive (latent) state eg. HIV
Epidemiology
The study of the outbreak and spread of infectious disease.
Used to plan and evaluate strategies to prevent the spread of the disease in the future.
Herd immunity
Vaccinations are used to increase the number of resistant hosts in a population, restricting the spread of a disease.
New infections are contained, as susceptible hosts are too dispersed amongst the population for transmission to occur.
Herd immunity threshold = the density of resistant hosts required to prevent an epidemic.
Protects individuals who are unable to be vaccinated.
Problems with treating parasitic diseases
Difficult to develop vaccines for parasites, as they are hard to culture in a lab, and parasites undergo rapid antigen change, making vaccine design very complex.
Host and parasite metabolism are often very similar. Drugs that target parasites may harm the patient, and may lead to resistance.
Most parasitic diseases are found in poorer parts of the world, so pharmaceutical companies don’t invest in them, as they can’t recoup their investment and make a profit.
Controlling parasites
Civil engineering projects, such as improving sanitation, reduces transmission of parasites with waterborne stages eg. Schistosoma
A co-ordinated vector control strategy will reduce transmission eg. mosquito nets, spraying houses with insecticide to control malaria.
Difficult in overcrowded unsanitary conditions (eg. refugee camps) and tropical climates which encourage rapid spread of parasites.
Benefits of improving parasite control
Reduction in child mortality
Better general health of children.
Children have more resources for growth and development, as they are not diverted to the parasites.
The population as a whole is healthier and intelligence increases.
