Chapter 13: Parasitism

Parasitism and Host Relationship

• Parasites typically feed on only one or a few host species, but host species have multiple parasite species.

How effective is parasitism as a life strategy

• Parasitism is an extremely effective life strategy, having evolved as many as 223 time in the animal kingdom

How many hosts do parasites usually attack?

Usually one or a few host species in their life cycle

Explain why many hosts species are host to more than one specialized parasite species

• It is unusual for any host to contain the full number of potential parasite species at once

• Graph included only helminth parasites (roundworm, tapeworm, flukes)

• In the graph, the unusual number of parasites from trees includes many species of insects that feed on the leaves and sap of trees (some consider these insect parasites)

Explain how parasites specialize on many different parts of the body both internally and externally

• This is possible because parasites tend to be much smaller than their hosts

• On possibility is that extreme specialization evolved to minimize competition among different species of parasites for resources provided by the host (a kind of resource partitioning).

Macroparasites

Large species such as arthropods and tape worms

Img: Whale tapeworm Tetragonoporusy calyptocephalus is a giant
parasite that lives in the intestines of whales and can reach 130 feet long

Microparasites

• Microscopic such as bacteria and viruses

• Virus is an Obligate intracellular parasite

obligate intracellular parasite

• Cannot replicate or reproduce outside of a host cell, relying instead on the host’s cellular machinery

• Ex: Virus

Ectoparasites

Live on the outer body of the host

Endoparasites

• Live inside their hosts, within cells or tissues, or in the alimentary canal

• Ex: Primary parasite vector and pathogen associated with Lyme disease Borrelia Burgdorferi bacteria

Lyme Disease Vector for Humans

• Blacklegged deer tick (Ixodes scapularis)

Lyme disease causative agent

• Borrelia burgdorferi

Lyme Disease Symptoms

• Chronic joint inflammation (Lyme arthritis), particularly of
  the knee.

• Neurological symptoms, such as facial palsy and
  neuropathy.

• Cognitive defects, such as impaired memory.

• Heart rhythm irregularities.

Life Cycle of Deer Tick (Ixodes Scapularis)

1. Y1 Spring- Uninfected six-legged larva hatches from egg and develops

2. Y1 Summer- Larva feeds on small animal, becoming infected, Borrelia burgdorferi is transmitted

3. Y1 Fall and Winter- Larva is dormant

4. Y2 Spring- Larva develops into eight-legged nymph

5. Y2 Summer Nymph feeds on animal or human, transmitting Borrelia burgdorfei

6. Y2 Fall and Winter- Nymph develops into adult tick

7. Y2 Fall and Winter- Adults feed on deer and mate, transmitting Borrelia burgdorfei

8. Y2 Spring- Female tick lays eggs

Overall: 2 yr life cycle and 3 blood meals, tick is infected by its first blood meal and can pass the pathogen to a human in its second

2 Advantages of Ectoparasitism

1. Ease of dispersal

2. Safe from host’s immune system

3 Disadvantages of Ectoparasitism

1. Vulnerability to natural enemies

2. Exposure to external environment

3. Feeding more difficult

3 advantages of Endoparasitism

1. Ease of feeding

2. Protected from external environment

3. Safer from natural enemies

2 disadvantages of Endoparasitism

1. Vulnerability to host’s immune system

2. Dispersal more difficult

3 significant challenges endoparasite dispersal presents

1. Often disperse through hostile environments between multiple hosts specific to certain life stages

2. Produces enormous numbers of offspring to compensate for very high mortality rates associated with their dispersal

3. Asexual reproduction is common due to low probability of finding sexual mates (they don’t tend to move once in body)

Primary host

• Also known as definitive host

• Is where the parasite reaches its adult stage and reproduces sexually

Secondary Host

• Also known as intermediate host

• Is where the parasite develops or undergoes a life cycle phase but does not reach sexual maturity

Example of how some parasites have evolved to alter the behavior of their hosts in ways that promote the completion of their life cycle

• Horsehair worms (Nematomorpha) manipulate host grasshoppers and cricket behavior to enter the water, where they drown

• The worms then emerge, breed, and lay their eggs

Example of how many parasites manipulate primary hosts to attract secondary hosts

• Leucochloridium paradoxum is a parasitic flatworm.

• Intermediate hosts are land snails.

• The pulsating, green broodsacs fill the eye stalks of the snail, purportedly attracting predation by birds, the flatworm’s primary host

• Snails eat eggs in bird feces.

CC How Toxoplasma gondii makes rodents fearless of cats

• In humans causes Influenza-like symptoms, swollen lymph nodes,
  headaches, fever, and fatigue, but symptoms are often not readily observable.

• As high as 30% of human population around world may have been exposed and may therefore be infected (called latent infection).

• Interesting fact: known to remove rodents' innate fear of cats.

• Toxoplasma gondii is another parasitic protozoa.

• Transmitted from feces of cats (the only known host in which reproduction occurs) to rodents and other mammals (including humans).

What is the host-parasite interaction representing a battle of

Parasite virulence and host defenses

4 Host defenses

1. Physical defenses- e.g tough skin

2. Immune system responses- Specialized cells to identify, engulf, and destroy microparasites

3. Encapsulations- Blood forms capsules around smaller parasites (common in insects)

4. Biochemical Defenses- Secondary compounds, common in plants

Immune system responses as host defense against parasites

Specialized cells to identify, engulf, and destroy microparasites

Encapsulation response as host defense against parasites

Blood forms capsules around smaller parasites (more common in smaller parasites)

Biochemical defenses as host response against parasites

Secondary compounds, common in plants

2 Parasite virulence (harm their hosts by decreasing their fitness)

1. Parasites try to multiply rapidly before an immune response can be deployed

2. Under selective pressure not to be so virulent as to kill their host, because the host must stay alive at least until transmitting offspring to new host.

3 ways and examples for how parasites can circumventing host’s immune system is common parasite survival strategy inside body

1. Parasites suppress the host’s immune system

   • HIV virus (Causes AIDS)

2. Parasites coat themselves with proteins that mimics the host’s own proteins

   • Ex: Schistosoma Mansoni, a parasitic blood fluke causing Schistosomiasis, or snail fever

3. Parasites coat themselves with novel proteins

   • Ex: Trypanosoma brucei, flagellated protozoan parasites that cause fatal African Sleeping sickness

Myxoma Virus

• Introduced in the 1950s and spread by mosquitoes proved to be an effective biological control agent, killing 99.8% of infected rabbits

CC How Introduction of Specialized Parasites to control invasive rabbit populations results in examples of coevolution

• Rabbits introduced by British to ranch in Victoria, Australia,1859.

• Years later, population exploded to hundreds of millions across continent, destroying pasturelands and threatening wool production.

• Myxoma virus introduced in 1950 and spread by mosquitoes proved to be an effective biological control agent, killing 99.8% of infected rabbits.

• Later outbreaks of the virus were less effective

Explain Coevolution Response Between Myxoma virus and Rabbits

• Decline in lethality of the myxoma virus in Australia resulted from evolutionary response in both the rabbit and virus populations

  1. Rabbits evolved resistance to virus (some populations had resistant genotypes)

  2. Myxoma virus evolved to be less virulent over time (like COVID and Influenza viruses in humans)

• Eventually, most surviving rabbits were resistant to virus

Examples of How Parasites are suspected of causing population cycles

• Grouse populations exhibited population crashes approximately every 4 years. The hypothesis was that these cycles were caused by parasites.

Explain the experiments that provided strong evidence that they were correct of parasites causing population cycles

• Controls, no parasites removed, cycles persist.

• B. Parasites treated/removed once at time indicated by*, cycles reoccur after treatment stops

• C. Parasites treated/removed twice at times indicated by*, cycles eliminated.

• Chytridiomycosis

• is an infectious disease in amphibians caused by the chytrid fungi Batrachochytrium dendrobatidis and Batrachochytrium salamandrivorans.

Explain how Chytrid fungus pose a new threat to amphibian populations

• Chytridiomycosis has been linked to amphibian population declines around the world and is spreading.

• The fungus is capable of causing low to medium rates of death in some amphibian populations and 100% mortality in others.

• No effective measure is known for control of the disease in wild populations.

Function of Simple SIR model for Host-Pathogen dynamics

provides important insights for controlling the establishment and spread of infectious disease.

When is the only time a disease can spread?

If density of susceptible host exceeds THRESHOLD DENSITY

Components of SIR Model For host-pathogen dynamics

• Breaks the host population into 3 subgroups-

  • S- density of susceptible individuals

  • I- density of infected individuals

  • m- recovered/death individuals

What is the SI variable meaning in SIR Model for host-pathogen dynamics

• Rate of susceptible encountering infected individual

• For a disease to spread, infected individuals must encounter susceptible individuals (S x I)

What is the β variable meaning in SIR Model for host-pathogen dynamics

• Transmission Rate

• (i.e how effectively the disease spreads from infected to susceptible individual)

βSI in SIR Model for host-pathogen dynamics

• Transmission rate of disease (β) x The rate of susceptible individual encountering infected (SI)

  • The density of infected individuals increases when disease is successfully transmitted (at rate βSI)

  • And decreases when infected individuals die or recover from disease

mI in SIR Model for host-pathogen dynamics

• The rate at which individuals die or recover is equal to the density of infected individuals multiplied by the death/recovery rate

• Rate of decrease in density of infections

S in SIR Model for host-pathogen dynamics formula

Susceptible density

I in SIR Model for host-pathogen dynamics formula

Infected density

β in SIR Model for host-pathogen dynamics formula

Transmission coefficent

m in SIR Model for host-pathogen dynamics formula

Death and recovery rate

(dI/dt) in SIR Model for host-pathogen dynamics formula

• Change in density of infected individuals at time

What does the SIR Model for host-pathogen dynamics model equation show:

• Rate of change in density of infected individuals at time t is equal to the rate of increase in density of infections minus the rate of decrease in density of infections.

• (dI/dt)= βSI-mI

• (dI/dt)= Rate of change in density of infected individuals at time t

• βSI= Rate of increase in density of infections

• mI- Rate of decrease in density of infections

When is disease established and spread in a population

• When density of infected individuals in a population increases over time

• This occurs when (dI/dt) > 0 or βSI- mI > 0

• Will become established and spread when the number of susceptible individuals (S) exceeds m/β

• Therefore disease is established as spread when S(t) = m/β

Threshold Density

• Formula: S(t)= m/β.

• To stop the spread of the disease, we need to keep the density of susceptible individuals (S) below

3 ways to control spread of disease

• To stop the spread of the disease, we need to reduce below threshold density, S(t)
  1. Lower the density of susceptible individuals (S)

  • Slaughter susceptible animals (a common practice when
    the disease is transmissible to humans)

  • Vaccines (extremely effective when available, but costly)

  2. Increase the recovery rate (m) by improving early detection
  and treatment.

  3. Increasing threshold density by decreasing transmission rate (β) by quarantining infected individuals which makes it difficult for ideas to spread