What are microparasites?

  • Fungal, bacterial, viral, and protozoan parasites

  • Small, typically fast reproduction, often lead to lasting immunity

Transmission modes

  • Can be transmitted many ways (water, direct, vectors)

  • Direct

    • direct contact (e.g., respiratory droplets)
    • sexual contact

  • Indirect

    • environment
    • water
    • vector

Bacterial microparasites

  • Unicellular prokaryotes (no mitochondria, unbound genetic material)

  • Can be intracellular or extracellular

  • Asexual reproduction (potential for horizontal gene transfer through plasmid transfer between cells)

  • Many bacteria are good (e.g., your gut bacteria)

  • e.g., black death (bubonic and pneumonic plague; Yersinia pestis), Cholera, Tuberculosis

A relevant bacterial microparasite


Cholera (Vibrio cholerae)

  • water-borne or contaminated food

  • acute diarrhoeal disease

  • severe symptoms can lead to death within hours

  • oral vaccine available, but still 1.3-4 million cases per year (21k - 143k deaths)

  • can be endemic or epidemic

Fungal microparasites

  • Rigid cell wall made of chitin

  • Vegetative growth via mycellium or budding

  • Hyphae can growth through host cells

  • Produce sexual or asexual spores

  • e.g., last of us? Athlete’s foot, ringworm, etc. Many more crop fungal pathogens (ergot and the Salem witch trials)

A relevant fungal microparasite

White nose syndrome (Geomyces destructans)

  • external fungal pathogen

  • grows well in cooler temperatures

  • death caused by dehydration or starvation (bats wake up early from hiberation)

  • transmitted directly and through environment

A relevant fungal microparasite

White nose syndrome (Geomyces destructans)

Viruses

  • Structurally simple = protein coat + genetic material (RNA or DNA)

  • RNA virsues has small genomes and high mutation rates, DNA viruses larger, more genes, and lower mutation rates.

  • Inert outside of hosts

  • Hijack host cell’s machinery to replicate (obligate intracellular parasite)

  • e.g., DNA: poxviridae (smallpox), herpesviridae (herpes, chicken pox)

  • e.g., RNA: flaviviridae (yellow fever, dengue), retroviridae (HIV)

A relevant virus

Dengue (DENV)

  • mosquito-transmitted (100-400 million infections per year)

  • fever, headache, nausea, vomiting, rash

  • Dengvaxia vaccine, but only for previously infected people where risk of reinfection is high

  • 4 types of dengue. No cross-type immunity, so reinfection happens and is bad

Another virus just for fun

West Nile Virus (WNV)

  • Most common mosquito-borne disease in USA

  • Infects birds (no bird to human transmission known)

  • Asymptomatic cases common

  • high fever, stiff neck, headache, stupor, coma, tremors, muscle weakness, vision loss, numbness

  • lifelong immunity

So I guess all viruses are just vector-borne?


  • No, just the coolest ones.

  • Influenza virus is directly transmitted and comes in a nice variety of flavors

Influenza

Influenza

Protozoan microparasites

  • Single-celled eukaryotes

  • Extremely diverse, loads of transmission modes and tissues infected

  • Can be intracellular or extracellular

  • Some host-specific, some incredibly broad host range

  • e.g., Plasmodium, Trypanosoma, Leishmania, etc.

A relevant protozoan

Leishmaniasis

  • 3 main forms (visceral, cutaneous, and mucocutaneous)

  • visceral is almost always fatal without treatment

  • transmitted by phlebotomine sandflies (90+ species can transmit)

  • associated with malnutrition, population displacement, poor housing, weakened immune function, etc.

  • 700k-1 million cases

  • Interaction with HIV means coinfection tends to produce really negative outcomes

The importance of vectors

  • All of those protozoans listed are vector-borne and many or most of the other examples were vector-borne

  • Vectors are incredibly important!

  • We will spend an entire week on vector-borne disease.

  • Get excited, because vectors add a neat layer of complexity onto disease systems

Density dependent transmission

  • Transmission depends on the density of susceptible and infected hosts (the well-mixed assumption of contact)

  • Transmission requires:

    • contact between individuals (\(cN\))
    • the right sort of contact (needs to be susceptible with an infected, right?)
    • successful parasite establishment (\(a\))

Density dependent transmission

  • For one infected individual, the probability that they encounter a susceptible individual is \(\frac{S}{N}\)

  • For all infected individuals in the population, this scales to \(I\frac{S}{N}\)

  • Transmission requires:

    • contact between a susceptible and an infected individual (\(c\))
    • successful parasite establishment (\(a\))

  • Transmission = \(caN\frac{S}{N}I\) = \(\beta SI\)

Frequency dependent transmission

  • Transmission depends on the number of contacts you have (e.g., sexually-transmitted infections)

  • Transmission requires:

    • contact between a susceptible and an infected individual (\(c\))
    • successful parasite establishment (\(a\))

  • Transmission = \(c\frac{S}{N}Ia\) = \(\beta\frac{SI}{N}\)

Transmission and the force of infection

Force of infection : per capita rate at which susceptible individuals get infected

  • But it’s different dependent on if the pathogen is frequency or density dependent, right?

\[ DD: \dfrac{dI}{dt} = \beta S \] \[ FD: \dfrac{dI}{dt} = \beta' S \]

but \(\beta \neq \beta'\)

and this is because \(\beta\) is a combination of contact \(c\) and parasite establishment \(a\).

Density dependent transmission assumes that you contact everyone


  • Density-dependent transmission = \(cN\frac{S}{N}Ia\)

  • …that \(cN\) is the contact of everyone with everyone.

How does contact scale with population density?

Threshold host density

Dallas et al. 2018 PRSB

What determines this threshold host density?

  • Recovery rate of infected hosts
  • Pathogen-induced mortality (virulence)
  • Pathogen survival in the environment (if environmentally-transmitted)

Why do we need to worry about ‘secondary infections’?

Dallas et al. 2018 PRSB

Would frequency or density dependent transmission result in lower threshold host density?


5 minutes to discuss this in small groups.

Maybe this is a tougher question than I intended

  • It really depends on where the host density threshold is

But let’s simplify things

  • Parasites with frequency-dependent transmission don’t really have a threshold host density in theory, but they often do in practice

    • Think about pathogen spread at very low host densities and refer back to 2-3 figures ago

  • This is a heady problem to think about, because we are acting like the same parasite can be transmitted as frequency or density dependent

  • And we aren’t even considering the pathogen challenge (are we just introducing 1 infected person into the population, or 10?)

One last note about this for clarity

Frequency-dependent transmission

\[ 0 < \beta \dfrac{SI}{N} - \gamma I \]

\[ \gamma < \beta \dfrac{S}{N} \]

  • Pre-outbreak, \(S=N\), so as host density never comes into the equation

Compare this with density-dependent transmission

\[ 0 < \beta SI - \gamma I \]

\[ \dfrac{\gamma}{\beta} < S \]

  • So host density is in the equation, where an outbreak will occur is \(\frac{\gamma}{\beta}\) is less than \(S\).

  • This will make more sense in the next lecture, where we will go a bit more into how we model infectious diseases, focusing on microparasites




End of lecture 1

What have we learned

  • A bit about microparasites and their different forms

  • A primer on how pathogens are transmitted (density/frequency dependent transmission)

  • A little bit of the fun math that we’ll use throughout the semester

Impacts of parasites

  • Population extinction

  • Invasive species (enemy release and biotic resistance)

  • Alter population dynamics

  • Weird knock-on effects (e.g., alter competitive landscape)

Population extinction (extirpation)

  • Do we expect parasites with density-dependent transmission to cause host extirpation?

  • Under what mechanisms could this happen?

    • stochasticity/small populations
    • non-DD transmission (inhomogeneous mixing)
    • reservoirs

de Castro and Bolker 2005 Ecology Letters

How often does parasite-induced extinction occur?

Invasive species (enemy release and biotic resistance)

  • enemy release : invasive species are less impacted by enemies than native species (lose parasites in process of invasion or parasites in invaded range not a good fit)

  • biotic resistance : invasive species more impacted by enemies than native species (can happen in a bunch of ways)

    • let’s think about some of the ways this could happen without leading to a net loss for both host species

Enemy release

  • European green crab Carcinus maenas has reduced parasite species richness (and infection prevalence) in its invasive range compared with its natural range

Biotic resistance

  • Eastern white pine (Pinus strobus) could not be introduced into Europe (after many attempts) because of a native blister rust (Cronartium ribicola) which is sustained by more tolerant indigenous European pines

Alter population dynamics

  • Red grouse dynamics in Britain are famously cyclic

  • The cause of these fluctuations is a nematode parasite whose impact is directly related to host demographic parameters (\(r_t\) and breeding mortality)

Hubson et al. 1998 Science

Take out parasite, take out cycling

Weird knock-on effects (e.g., alter competitive landscape)

  • Population dynamics (growth is determined by birth and death)

  • \(N = B - D\)

  • but parasites can result in additional mortality (\(N=B-D-\omega\))

  • this extra mortality can cause competition between species to change, or affect food web dynamics (e.g., deer infected by chronic wasting disease alter wolf population dynamics)

Parasite-mediated competition

Microparasite dynamics in host populations

  • Outbreaks: Sudden increase in disease in a population that forms epidemic curve

  • Sequential epidemics: Multiple waves or peaks of infection

  • Endemic parasites: Increase in prevalence that eventually settles to some equilibrial amount of infection

Outbreaks

Sequential epidemics

Endemic parasites

Modeling microparasite infections

  • To understand, forecast, and mitigate infectious disease, we need to be able to model them (or at least fit a model to them).

  • statistical modeling : fitting a model to data to gain inference or prediction.

  • phenomenological modeling : building a model from first principles to describe a system’s behavior. Can then be fit to data.

Some examples to help distinguish

  • Campylobacter: bacterial pathogen (infection comes from animals or animal feces, mainly poulty)

Don’t eat chicken liver pâté at holiday parties

O’Leary et al. 2009 Epidemiology and Infection

Campylobacter cases in Germany from 2001-2011

Statistical modeling

Fit a statistical model just based on case counts over time

  • good for exploring periodicity in infections
  • could be useful for forecasting

How can simple models produce all of these complex patterns?

  • Next lecture we’ll be going over modeling infectious disease

  • Most of the models we will go over produce outbreak-like dynamics (epidemics)

Before next class, think about when you would expect to see sequential epidemics or endemic infections

Modeling infectious disease : S-I-R

S : susceptible individuals

I : infectious individuals

R : recovered (and immune) individuals

Costs of parasitism do not have to involve death

S-I-R model

\[ \begin{aligned} \frac{dS}{dt} &= -\beta SI \\ \frac{dI}{dt} &= \beta SI - dI \\ \frac{dR}{dt} &= dI \end{aligned} \]

  • Is this density or frequency dependent transmission?

SIR curves

S-I-R model

  • frequency-dependent transmission

\[ \begin{aligned} \frac{dS}{dt} &= -\beta \dfrac{SI}{N} \\ \frac{dI}{dt} &= \beta \dfrac{SI}{N} - dI \\ \frac{dR}{dt} &= dI \end{aligned} \]

Host population size still matters for frequency-dependent transmission

  • But in terms of infection prevalence, not in terms of pathogen invasion

  • This also makes the odd assumption that there is no recovery of infected hosts

If we include a recovery term, we see shifted epidemic curves

  • In the next lecture, we’ll focus much more on density-dependent transmission and the underlying modeling framework.

  • We’ll also be incorporating further realism into the simple SIR model to think about epidemics and endemic disease