Spatial Hetergeneity

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From the course by The Pennsylvania State University

Epidemics - the Dynamics of Infectious Diseases

590 ratings

The Pennsylvania State University

Epidemics - the Dynamics of Infectious Diseases

590 ratings

Not so long ago, it was almost guaranteed that you would die of an infectious disease. In fact, had you been born just 150 years ago, your chances of dying of an infectious disease before you've reached the tender age of 5 would have been extremely high. Since then, science has come a long way in understanding infectious diseases - what they are, how they spread, and how they can be prevented. But diseases like HIV/AIDS, Malaria, Tuberculosis, or the flu are still major killers worldwide, and novel emerging diseases are a constant threat to public health. In addition, the bugs are evolving. Antibiotics, our most potent weapon against bacterial infections, are losing their power because the bacteria are becoming resistant. In this course, we'll explore the major themes of infectious diseases dynamics. After we’ve covered the basics, we'll be looking at the dynamics of the flu, and why we're worried about flu pandemics. We'll be looking at the dynamics of childhood diseases such as measles and whooping cough, which were once considered almost eradicated, but are now making a comeback. We'll explore Malaria, and use it as a case study of the evolution of drug resistance. We'll even be looking at social networks - how diseases can spread from you to your friends to your friends' friends, and so on. And of course we’ll be talking about vaccination too. We’ll also be talking about how mobile phones, social media and crowdsourcing are revolutionizing disease surveillance, giving rise to a new field of digital epidemiology. And yes, we will be talking about Zombies - not human zombies, but zombie ants whose brains are hijacked by an infectious fungus. We're looking forward to having you join us for an exciting course!

From the lesson

Epidemiology

Where humans live and how they are connected to each other, have strong effects on how infectious diseases can spread. In this module, you will learn about some of the related key concepts of epidemiology. After looking at some fascinating history, we’ll learn about social networks as the ultimate “road map” on which diseases can travel and we’ll talk about how the structure of the network can influence disease dynamics. After that, we’ll cover three topics that all affect infectious disease epidemiology in dramatic ways: human transport systems, population density and so-called superspreaders - individuals who can spread a disease to dozens or even hundreds of other individuals. We’ll close by identifying what information is required for disease surveillance.

Spatial Hetergeneity5:31

Movement and Modern Transportation5:59

Surveillance and Disclosure5:39

Co-Infection Consequences10:25

Meet the Instructors

Dr. Ottar N. Bjornstad
Professor of Entomology and Biology
Department of Biology
Dr. Rachel A. Smith
Associate Professor
Department of Communication Arts & Sciences and Human Development & Family Studies
Dr. Mary L. Poss
Professor of Biology
Department of Biology
Dr. David P. Hughes
Assistant Professor of Entomology and Biology
Department of Biology
Dr. Peter Hudson
Willaman Professor of Biology
Department of Biology
Dr. Matthew Ferrari
Assistant Professor of Biology
Department of Biology
Dr. Andrew Read
Alumni Professor in the Biological Sciences, and Professor of Entomology
Center for Infectious Disease Dynamics
Dr. Marcel Salathé
Assistant Professor of Biology
Department of Biology

Emergence of new human pathogens are often associated with rural areas, where

people have frequent contact with animal reservoirs of so as to invite infections.

Cities, in contrast, are often the reservoirs,

or core areas, for many established human pathogens.

Cities can provide more robust chains of transmission.

Both because of increased contact rates and because of the greater

supply of susceptible individuals.

Cities are essential arenas for both the evolution and ecology of human infections.

It is believed that many important pathogens only established

in humans following the neolithic revolution around 10,000 years ago,

when early humans made the first settlements, that eventually

grew into early cities some three to 5,000 years ago.

This includes species jumps by smallpox, tuberculosis, measles,

whooping cough and probably most other acute immunization

infections that would rapidly fired out

in the spars pre-settlement human populations.

Transmission in cities was particularly be rampant in the beginning of

the industrial revolution during the early part of the 19th century.

Workers often lived in very crowded unsanitary conditions, in

which contagent of tuberculosis, typhoid and cholera was rampened.

Tuberculosis alone causing up to 25% of all deaths In

many cities.

In early industrialized cities like Liverpool and Manchester, the death rate

from TB was ten times that of the surrounding rural areas.

The death rate from childhood infections, like

measles and whooping cough, we four times higher.

Mortality rates on the whole were 50% higher than the national average.

Sanitation, vaccination, and urban health infrastructure have

greatly altered the abysmal situation of the past.

However, big cities still play an important role in

the dynamics of many infections Most epidemics of immunizing

infections, for example, quickly burn out in smaller towns

or villages because they run out of susceptible individuals

to sustain the chain of transmission.

Such infections can only persist in communities above a certain size.

Or really, in communities in which the

birth rate of un-vaccinated children is sufficiently high.

Dynamically speaking, this leads to what is called island-mainland

metapopulation dynamics. In ecology, a metapopulation is a group of

local populations or communities connected by infrequent movement amongst them.

In island-mainland epidemics, the pathogen retreats to

a few big, cool cities during inter-epidemic periods,

allowing the susceptible populations to build up in smaller communities.

Intermittently, when susceptibles are numerous enough,

For the effective reproductive number to

exceed one, the pathogen can spread

through smaller communities to cause broad-scale epidemics.

This type of dynamic is clearly illustrated by pre-vaccination measles.

In interepidemic periods, measles was only present in less than ten big cities.

During the major epidemic that happened every two

years or so, measles was present virtually everywhere.

The spread out of the big cities

happens in a very characteristic hierarchical fashion, where,

on average, the timing of epidemic happens in

an order of descending size and increasing isolation.

This timing comes about because of key characteristics

of human mobility, by which movement is more frequent

between big cities and more frequent between communities close together.

We see similar patterns of what is called hierarchical diffusion

in many other childhood infections as well as seasonal influenza.

Well this type of spread is inherently random.

We can predict a relative risk of outbreaks

using the circle gravity models of human mobility.

Today in many European countries vaccine cover is high enough

that no cities are big enough for sustained transmission of measles.

However in contrast to the Americas, where measles is eliminated.

Measles persists regionally by jumping from city to city.

Causing epidemics that quickly die out locally.

In disease ecology, we call this metapopulation persistence,

as opposed to the more conventional local persistence, that

relies on unbroken chains of transmission in each host community.

Rabies in raccoons and plague in prairie dogs are examples

of animal diseases that only can persist at the metapopulation level.

Since the movement of wild animals are simpler

and do not rely on complicated human transportation networks.

We often see spatial waves will spread of

rabies and plague, that are reminiscent of forest fires.

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