Review

Research review
Blackwell Publishing Ltd

Modelling disease spread and control in

networks: implications for plant sciences

Author for correspondence:
Marco Pautasso
Tel: +44 (0)20 759 42816
Fax: +44 (0)20 759 42669
Email: m.pautasso@ic.ac.uk
Received: 13 December 2006
Accepted: 9 January 2007
Mike J. Jeger1, Marco Pautasso1, Ottmar Holdenrieder2 and Mike W. Shaw3
1
Division of Biology, Imperial College London, Wye Campus, Kent TN25 5AH, UK; 2Institute of
Integrative Biology, Department of Environmental Sciences, Eidgenössische Technische Hochschule,
8092 Zurich, Switzerland; 3The University of Reading, School of Biological Sciences, Lyle Tower,
Whiteknights, Reading RG6 6AS, UK

Summary

Key words: complex networks, disease
management, epiphytotics, landscape
pathology, network structure, plant
pathogens, small-world, spatial dispersal.
Networks are ubiquitous in natural, technological and social systems. They are of
increasing relevance for improved understanding and control of infectious diseases
of plants, animals and humans, given the interconnectedness of today’s world.
Recent modelling work on disease development in complex networks shows: the
relative rapidity of pathogen spread in scale-free compared with random networks,
unless there is high local clustering; the theoretical absence of an epidemic threshold
in scale-free networks of infinite size, which implies that diseases with low infection
rates can spread in them, but the emergence of a threshold when realistic features
are added to networks (e.g. finite size, household structure or deactivation of links);
and the influence on epidemic dynamics of asymmetrical interactions. Models
suggest that control of pathogens spreading in scale-free networks should focus on
highly connected individuals rather than on mass random immunization. A growing
number of empirical applications of network theory in human medicine and animal
disease ecology confirm the potential of the approach, and suggest that network
thinking could also benefit plant epidemiology and forest pathology, particularly in
human-modified pathosystems linked by commercial transport of plant and disease
propagules. Potential consequences for the study and management of plant and
tree diseases are discussed.

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doi: 10.1111/j.1469-8137.2007.02028.x

of the relations between them. From both perspectives, networks

Introduction
Much scientific work is currently focusing on the properties
of networks (see Barabási & Albert, 1999; Newman, 2003;
papers cited therein). From a physical point of view, networks
may involve transport of energy, matter or information. From
a mathematical standpoint, networks are sets of elements and
are models applicable to a wide variety of natural, technological
and social systems (e.g. Strogatz, 2001; Albert & Barabási,
2002; Table 1). Networks can be of interest to plant scientists
when they are formed by a physical structure, when they refer
to abstract relationships between connected entities (e.g. different
species), and when they underline processes or flows in a structure.

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Table 1 Examples of natural, technological and social networks that have been the object of recent analyses

Network Type Examples of references

Natural
Prebiotic mutually catalytic pathways V Shenhav et al. (2005)
Microbial phylogenies (horizontal and vertical transfer of genes between microbes) SF Kunin et al. (2005)
Cellular and metabolic dynamics (interactions of cellular components and biochemical molecules) SF Jeong et al. (2000);
Albert (2005)
The topology of food webs (who eats whom in ecological communities) V Dunne et al. (2002);
Woodward et al. (2005)
Neural networks (the connections between neurons of e.g. the nematode SW Watts & Strogatz (1998);
Caenorhabditis elegans) Humphries et al. (2006)
Ant nests (a set of chambers interconnected by galleries) N Buhl et al. (2004)
Amphibian meta-populations in ponds SF Fortuna et al. (2006)
Bats roosting in hollow trees SF Rhodes et al. (2006)
Foraging walks of primates SF Boyer et al. (2006)
Spatially remote thunderstorms SW Yair et al. (2006)
The Earth’s climate system (e.g. the correlations of monthly pressures on a 5 by 5 degrees grid) SW Tsonis & Roebber (2004)
Earthquake networks (links between strongly correlated earthquake events) SF Baiesi & Paczuski (2005)
Syllable and word webs (the co-occurrence of syllables in words and of words in sentences) SF, SW Cancho & Solé (2001);
Soares et al. (2005)
The decomposition of even numbers into two prime numbers (following the Goldbach conjecture) SW Chandra & Dasgupta (2005)
Technological
Railways (stations and connecting trains) SW Sen et al. (2003)
Urban street networks (streets and intersections) SW Jiang & Claramunt (2004)
Electric power grids (power generators, substations, high-voltage transmission lines) SF Amaral et al. (2000);
Chassin & Posse (2005)
Air transport (airports and connecting flights) V Barrat et al. (2004a);
Guimerá et al. (2005)
The Internet (transit backbone providers and their nodes) V Gorman & Malecki (2000);
Pastor-Satorras et al. (2001)
Computing grids (a set of processors connected by some kind of communication network) V Costa et al. (2005)
Software maps (the topology of complex software systems) V Valverde & Sole (2005)
Electronic circuits in computers (logic gates connected by wires) SW Cancho et al. (2001)
Social
Family networks (who is related to whom) SF Coelho et al. (2005)
Friendship groups (who knows whom) SW Milgram (1967);
Amaral et al. (2000)
Bookworm contacts (book buyers spreading recommendations) SF Sornette et al. (2004)
Links between Wikipedia articles SF Capocci et al. (2006);
Zlatic et al. (2006)
The World Wide Web (links to web pages) V Adamic (1999);
Bornholdt & Ebel (2001)
Virtual learning communities (cultural transmission as contagion) ? Giani et al. (2005)
Medieval heresies and inquisition SF? Ormerod & Roach (2004)
Committees (who is in a meeting with whom) ? Porter et al. (2005)
Telephone calls (sets of people with whom a telephone user communicates) SF Xia et al. (2005)
Email patterns (electronic messages between email addresses) SF Ebel et al. (2002)
Co-authorship groups (who does research with whom) SF Newman (2001);
Barber et al. (2006)
Citation webs of scientists (who cites whom) SF Seglen (1992)
Terrorist groups (webs of perpetrators of terror attacks) V Qin et al. (2005)
Financial fluctuations (e.g. the cross-correlations of stock prices) SF Boginski et al. (2005)
Innovation flows (e.g. the flow of technological improvements from firm to firm) SF Di Matteo et al. (2005)
Human movements (tracked for instance following the dispersal of bank notes) SF Brockmann et al. (2006)
The UK horse racing network SW Christley & French (2003)
The world trade web (trade relationships between different countries) V Serrano & Boguñá (2003)
Sexual partnerships V Kretzschmar (2000)

Network types (SF, scale-free; SW, small-world; V, various types; N, none of the previous types) are assigned on the basis of the references
provided and do not rule out the possibility that other studies of networks of a similar nature may suggest a different structure. For other
references the reader is referred to reviews by, for example, Albert & Barabási (2002), Dorogovtsev & Mendes (2002) and Newman (2003).

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Table 2 Idealized network types discussed in the text (see Fig. 1 for a visual representation)

Type Description Properties Examples of references

Local Neighbourhood connectivity
(typically regular lattices)
Random Nodes connected with
probability P (Erdos–Renyi network)
Small-world Local network rewired with
shortcuts (Watts–Strogatz network)
Scale-free Nodes preferentially connecting
to hubs (Barabási–Albert network)
High clustering, Harris (1974); Keeling & Eames (2005);
high path length Shirley & Rushton (2005a)
Low clustering, Erdos & Renyi (1960); Bollobás (1985);
low path length Roy & Pascual (2006)
High clustering, Watts & Strogatz (1998); Barrat & Weigt (2000);
low path length Moore & Newman (2000)
Proportion pk of vertices Barabási & Albert (1999); Balthrop et al. (2004);
connected to k other Hwang et al. (2005); Newman (2005a)
vertices drops with increasing
k as k–α for some constant α

Network theory (e.g. Bollobás, 1979; Chartrand, 1985;

Chen, 1997) has many practical biological applications in
plant sciences, for example biochemical networks (Aloy &
Russell, 2004; Arita, 2005; De Silva & Stumpf, 2005; Green
& Sadedin, 2005; Proulx et al., 2005; Sweetlove & Fernie,
2005; Uhrig, 2006), which form much of the focus of what
is now termed systems biology. But epidemiological studies
are also interesting dynamical problems in a system of con-
nected entities (e.g. Matthews & Woolhouse, 2005; Zheng
et al., 2005). A number of papers have summarized recent
work modelling the spread of diseases in networks (to which
we refer for more details, elaboration and perspectives; e.g.
Wallinga et al., 1999; Watts, 1999; Koopman, 2004; Keeling
& Eames, 2005; Keeling, 2005b,c; Shirley & Rushton,
2005a; May, 2006; Parham & Ferguson, 2006). However, most
of this work has focused on human and animal diseases, thus
raising the question of whether a similar approach may also be
beneficial in plant and forest pathology.
The relevance of network theory to the epidemiology of
plant diseases is demonstrated by the growing literature on:
how landscape patterns affect the spread and establishment of
plant pathogens; large-scale site topographic, climatic and
edaphic characters predisposing to plant disease risk; and host
and pathogen genetic variation across their geographical
distribution. New genetic tools enable a much more precise
study of the dispersal of organisms on a geographic scale (e.g.
Banke & McDonald, 2005; Garrett et al., 2006; Stukenbrock
et al., 2006), and many questions in large-scale epidemiology
can be conveniently framed in terms of network theory. In
this review, we recapitulate important results of modelling
work on disease spread and control in networks, present
empirical studies applying network theory to a number of case
studies of human and animal pathologies, and discuss poten-
tial consequences for plant disease epidemiology (e.g. Gilli-
gan, 2002; Jeger, 2004; Burdon et al., 2006) and for landscape
pathology, which is the study and management of tree diseases
on a larger scale than previously common and making use of
the tools of landscape ecology (e.g. Geils, 1992; Holdenrieder
et al., 2004; Lundquist & Hamelin, 2005; Pautasso et al.,
2005).
Modelling work
Epidemiological approaches based on networks study indivi-
duals and their contacts as a set of vertices (also known as
nodes, i.e. susceptible/infected entities) and connecting edges
(links and infection events) (e.g. May & Lloyd, 2001; Pastor-
Satorras & Vespignani, 2001a; Newman, 2002). The contact
patterns between susceptible and/or infected individuals form
a network, which can be classified into various types (Table 2;
Fig. 1). In the approach most obviously related to network
theory, disease has been modelled on regular lattices, where
the probability of infection being passed to neighbouring cells
on a grid can be constant (zero-dimensional models, or mass-
action mixing; e.g. Anderson & May, 1991; Filipe & Maule,
2004) or random (epidemics in random graphs; e.g. Barbour
& Mollison, 1990), or can decrease as a certain function of the
distance from an infected cell (typically producing travelling
waves as in continuum models; e.g. Marchand et al., 1986;
Zadoks & Van den Bosch, 1994; Van den Bosch et al., 1999;
Russell et al., 2004). For plants, a further distinction can be
drawn between models that operate in a landscape of a more
or less fragmented natural environment and those studying
the behaviour of trade-based networks.
However, real populations rarely fall exactly into one of
these idealizations, being neither completely artificial nor
natural, and neither perfectly well-mixed, nor completely
random, nor located on regular lattices (e.g. Mollison, 1977;
Shaw, 1994; Kuperman & Abramson, 2001; Blyuss, 2005).
Networks where connectivity is neither local, nor regular nor
random but something in between these three extremes are
dubbed ‘small-world’ networks, because the shortest path
length between individuals increases only logarithmically
with increasing size of the network (Table 2; Fig. 1). It is on
these small-world networks, where global distances are low
and local interconnectedness (clustering) is high (Petermann
& De Los Rios, 2004; Roy & Pascual, 2006), that many
modellers have focused their recent epidemiological work.
Another type of network that has been the object of much
investigation is the scale-free network. In scale-free networks,
the probability that a given node has k connections follows an

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inverse power-law distribution (Table 2; Fig. 1). This is called
the degree distribution of the network. Illustrations of such a
scale-free distribution in real-world networks can be found in
many recent papers (e.g. Shirley & Rushton, 2005b; Barber
et al., 2006; Montoya et al., 2006). Most scale-free networks
have small-world properties (e.g. Amaral et al., 2000), but
there are scale-free networks with low clustering, which are
thus not small-worlds, and there are small-world networks
that are not scale-free (see e.g. Jiang & Claramunt, 2004;
Humphries et al., 2006). A particular class of networks with
both scale-free and small-world properties is called Apollonian
networks (e.g. Andrade et al., 2005), but there are many kinds
of network with both scale-free and small-world properties
that are not Apollonian (e.g. Matsuyama et al., 2005; Palotai
et al., 2005). Each type of complex network described here
can be embedded in space (e.g. Rozenfeld et al., 2002;
Barthélemy, 2003; Morita, 2006). The distance between
two nodes will be reflected in the strength of the connection
between them, although it will not necessarily be the only
determinant. This is of particular interest to plant scientists,
as a plant lives in a single physical location.
Epidemiological models in networks can be roughly sub-
divided into those pertaining to disease spread and those
pertaining to disease control, although the interrelations are
obvious. Throughout, for ease of readability, mathematical
assumptions and notations of models are not reported from
the original papers, to which interested readers are referred.
Disease spread in networks
Recent work on disease spread in networks shows that the
probability of an epidemic occurring following an initial
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Fig. 1 Four basic kinds of network structure:
(a) local, (b) random, (c) small-world, and
(d) scale-free. Graphs are networks of 100
individuals with a constant number of links.
The circular layout does not reflect the spatial
arrangement of nodes.
infection is influenced by the contact structure in the first
phases of the epidemic (Gallos & Argyrakis, 2003; Brauer,
2005; Saramäki & Kaski, 2005). Depending on where it
originated, the first phase of an epidemic in a scale-free
network is often marked by super-spreading events, in which
a few infected entities with high numbers of connections are
responsible for the vast majority of infections (Barthélemy
et al., 2004; Brauer, 2005; Duan et al., 2005; James et al.,
2007). An immediate finding is thus that infectious diseases
can spread more easily in scale-free and small-world networks
than in regular lattices (e.g. Watts & Strogatz, 1998; Kuperman
& Abramson, 2001) and random networks (Kiss et al., 2006a;
Matthäus, 2006), although spread is less predictable because
of more stochasticity during the very early stages of the epidemic.
High degrees of local clustering can lead to a less than
exponential spread of diseases even at the very beginnings of
epidemics (Szendrøi & Csányi, 2004; Verdasca et al., 2005).
A second major result of models is that, in small-world
networks, the threshold for an epidemic to occur decreases as
a power-law with increasing number of shortcuts (long-
distance infections) (Zekri & Clerc, 2001). As a result of the
heterogeneity in the number of links per node, epidemics in
scale-free networks of infinite size theoretically never die out,
no matter how low the basic reproduction rate is (Pastor-
Satorras & Vespignani, 2001b; Moreno et al., 2002b; Boguñá
et al., 2003; Barthélemy et al., 2005). Therefore, in scale-free
networks, in order to correctly estimate R0, some measure of
the variance in the degree distribution of contacts is needed
(Woolhouse et al., 2005; Ferrari et al., 2006; Green et al., 2006;
May, 2006). The concept of a basic reproduction number R0
comes from studies of disease spread in homogenous landscapes
(e.g. Heesterbeek, 2002; Brauer, 2005; Green et al., 2006; for

plant epidemiology, e.g. Jeger, 1986; Jeger & van den Bosch,
1994). It is defined as the number of secondary infections
caused by a single infective individual introduced into a
wholly susceptible population, and depends normally on: the
number of potentially infectious contacts per individual; the
probability of infection per contact between infectious and
susceptible individuals; and the duration of infection (e.g.
Giesecke, 1994; Hethcote, 2000; Lloyd-Smith et al., 2005;
May, 2006). If R0 is less than 1 in a homogeneous population,
epidemics fail to establish.
In networks in which the probability of a node having a
certain number of contacts decreases exponentially as the number
of contacts increases, which are therefore not scale-free, a thresh-
old R0 exists even in case of an infinite size (Pastor-Satorras
& Vespignani, 2001a). This is because the transmissibility
scales in non-scale-free networks with the average degree
(number of connections), whereas in scale-free networks it
scales with the variance of the degree distribution. For an epi-
demic threshold to be absent (in the infinite size limit, and
with the exponent of the power-law smaller than 3; see
Table 2), the connectivity of the network must thus be scale-
free. A scale-free connectivity (i.e. a linear decrease in log-log
space of the number of links per node with increasing number
of nodes in a network) implies the existence of hubs, or highly
connected nodes. These hubs are largely responsible for the
observed differences between processes (not only epidemio-
logical) modelled on scale-free networks and other kinds of
complex networks (e.g. Amaral et al., 2000). The key role of
hubs is corroborated by the finding that not only is the epi-
demic threshold lower in scale-free networks, but the time
needed for equilibrium levels of infection to be reached is
shorter (e.g. Shirley & Rushton, 2005a).
Work demonstrating the absence of an epidemic threshold
in scale-free networks of infinite size is not a mathematical
irrelevance, because, although scale-free networks of finite size
(with cut-offs at the lower and higher ends of the distribution
of connections) have thresholds, neglecting long-distance
connectivity still leads to an overestimation of the epidemic
threshold in finite populations (May & Lloyd, 2001; Pastor-
Satorras & Vespignani, 2002a; Joo & Lebowitz, 2004; Hwang
et al., 2005; Ying et al., 2005). Whether or not epidemic
thresholds are really lower in real-world heterogeneous land-
scapes than in homogenous ones is an interesting question
and requires field work for it to be tested also empirically.
Whether or not scale-free networks are relevant for plant
meta-populations will be discussed in detail later in the review
(see ‘Potential implications for plant and forest pathology’).
Suffice it to say for now that, although plant networks are finite
(the world’s circumference has an order of magnitude of 107 m,
and individual leaves of diseased plants are around 10−2 m,
which would give potentially 10 orders of magnitude), if an
epidemic were to spread around the world during a period
substantially longer than its time of local development, then
it might not be too far-fetched to apply results from models
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Research review Review 283
of scale-free networks of infinite size to plant networks in
today’s globalized world. It would also be interesting to know
how relevant the distinction established by these thresholds
is for real epidemics. These might be theoretically unstable, but
last sufficiently long to make the threshold irrelevant in practice.
A third take-home message is that more complicated models
also have an epidemic threshold. Thresholds are predicted
in networks with high local clustering (Eguíluz & Klemm,
2002), in models taking into account differences in the rate of
infection for individuals with different connectivity (Olinky
& Stone, 2004), and, depending on the initial density of
infection, in models of disease spread in scale-free networks
created by the deactivation of links with probability inversely
proportional to their number of connections (Moreno &
Vázquez, 2003). Similarly, the combined effects of ageing
(older individuals in a network differing in their susceptibility)
and removal of links (dead individuals may no longer be con-
nected to susceptible ones) on epidemic dynamics in scale-free
networks lead to a critical value of effective links in the net-
work below which only local spread of disease takes place
(Chan et al., 2004; see also Amaral et al., 2000). The epidemic
threshold in community networks (where there are groups of
individuals with more connections between them than with
individuals outside the group), however, is still lower than in
a random network, other things being equal (Liu & Hu, 2005).
This issue is of relevance for plant diseases, because plants
in a field, forest or nursery may be at risk of infection from
pathogens present on plants in the same location, but also from
longer distance movements of disease propagules from other
fields, forests or nurseries (e.g. Parnell et al., 2006; Shaw et al.,
2006).
However, in scale-free networks with household structure
(which enables a distinction between infection among and
within households (Bian, 2004); for plant meta-populations,
the concept of household may be conveniently thought of in
terms of farms, pathosystems, or pathoregions (see Holden-
rieder et al., 2004)), models predict that a disease can spread
through the network even if the recovery rate in single house-
holds is greater than the local infection rate (Liu et al., 2004).
However, as for homogenous networks, Grabowski & KosiNski
(2004) have found that in household networks disease spread
is slower when there is much local clustering. The same
authors have reported that, in these household network
models, diseases with a lower rate of spread have a greater
probability of surviving endemically. This finding is in agree-
ment with the general theory of disease spread when there is
a high variance in contacts between individuals (Anderson &
May, 1991). Household structure also introduces into models
an asymmetry between individuals inside groups and individuals
connecting groups, with a higher probability of infection
from connecting individuals to those within a household than
vice versa (Meyers et al., 2003).
A fourth general finding is thus that asymmetries can have
an influence on disease spread in networks. It is known that
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models with symmetrical interactions are often unrealistic
approximations of real systems (e.g. Bauch & Galvani, 2003;
Bascompte et al., 2006; Chavez et al., 2006). Many real patho-
systems present heterogeneities or asymmetries in the flow of
disease propagules carried by different links (e.g. Dall’Asta,
2005; Yan et al., 2005). A number of studies have started
investigating the spread of pathogens in directed networks of
various kinds (e.g. Newman et al., 2001; Schwartz et al., 2002;
Boguñá & Serrano, 2005; Meyers et al., 2006). For plants,
directed networks may be of relevance, for instance, in the
case of the trade among nurseries, garden centres and retail
centres, where the probability of movement from a certain
nursery to a given garden centre will tend to differ greatly
from the probability of movement in the reverse direction.
In many real-world examples, not only the number and
direction of connections of different nodes may be heteroge-
neous, but also their strength. Recent work has started to take
into account the variation in intensity of different links (e.g.
Yook et al., 2001; Barrat et al., 2004b; Jezewski, 2005), but
investigations of the implications of including weight in
models of disease spread and control in complex networks are
still in their infancy (e.g. Wu et al., 2005; Dall’Asta et al.,
2006). Intuitively, when higher connectivity strength per link
is assigned to highly connected individuals, the findings dis-
cussed for nonweighted scale-free networks will tend to be
present even more strongly. But it would be interesting to
know whether or not (and under which conditions) strong
links for the many nodes with few connections can cancel out
the effect of hubs if these have weak links. For plant diseases,
hubs with weak links may be a realistic model of control targeted
exclusively at plant movements from and to highly connected
traders, while strong links to many other nodes would be an
appropriate model if commercial growers with many customers
also tended to sell significantly more plants than small-scale
retailers with few connections.
Disease control in networks
A number of consequences for disease management can be
inferred from modelling work on disease spread in networks.
First, models show that random immunization of even a
high proportion of individuals is not an effective strategy to
control an epidemic operating in scale-free networks. This
result follows from the theoretical absence of an epidemic
threshold in scale-free networks with infinite variance in
connectivity: in this case, immunity is not conferred even by
high densities of randomly immunized individuals (e.g. Pastor-
Satorras & Vespignani, 2002b; Zanette & Kuperman, 2002;
Takeuchi & Yamamoto, 2005). In networks with small-world
properties, as a result of the effect of shortcuts, the influence
of an untargeted immunization protocol is generally lower
than when only local infection is possible (KosiNski &
Adamowski, 2004). In a botanical context, protection may be
conferred by biological control or fungicides at the level of the
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individual field, and by the intermixing of resistant varieties
and species at the landscape level.
Rather than random immunization, when disease spreads
on a scale-free network, an effective control strategy should
immunize highly connected nodes (e.g. Pastor-Satorras &
Vespignani, 2002b; Zanette & Kuperman, 2002; Liu et al.,
2003; Chang & Young, 2005; Hwang et al., 2005; Lloyd-
Smith et al., 2005). Models suggest that the more strategies
focus on immunization of highly connected individuals, the
more likely they are to bring under control an epidemic
spreading on a scale-free network, and the cheaper a successful
strategy will be (Dezsø & Barabási, 2002). These models
predict that in a finite population, even with small-world
properties, above some critical immunization level the disease
is confined locally (Zanette & Kuperman, 2002). Moreover,
just as local clustering slows down the spread of disease in
networks (see ‘Disease spread in networks’), a lower efficiency
in contact tracing is required to control disease in a clustered
network, other things being equal (Eames & Keeling, 2003).
For plant diseases, contact tracing often translates into removal
of infected plants and the containment of further pathogen
spread across a dispersal network through quarantine
measures. Even without human intervention, it is a common
observation – for example, in the saprotrophic invasion of
the soil-borne pathogen Rhizoctonia solani – that patches of
susceptible plants can remain uninfected because they are
surrounded by immune individuals (e.g. Jeger, 1989; Bailey
et al., 2000; Sander et al., 2002).
A number of parameters have been analysed to enable the
identification of highly connected individuals in small-world
and random networks: degree (number of contacts), between-
ness (a measure of the probability of an individual being on
the path between other individuals), shortest-path between-
ness (the same, but for the shortest path), and farness (the sum
of the number of steps between an individual and all other
individuals). Degree, the network parameter most easily
measured, was found to be at least as good as the other metrics
in identifying highly connected individuals and thus in
predicting risk of infection (Christley et al., 2005). This result
is to be expected from the common finding in real-world net-
works that the betweenness of a node is positively correlated
with the degree of the node (e.g. Lee et al., 2006).
From a practical point of view, however, there is often only
limited knowledge at the beginning of an epidemic outbreak
about the number of connections single individuals have
(Dybiec et al., 2004). For many airborne diseases, a substantial
fraction of contacts may be untraceable (Eames & Keeling,
2003). When contact tracing is possible in theory, if latent
periods are short there may not be time in practice to trace the
contacts of connected and infected individuals (Huerta &
Tsimring, 2002; Kiss et al., 2005). But in plant epidemiology,
where long latency periods are common, it may also be diffi-
cult to trace contacts. Researchers have thus tried to identify
control strategies that do not require pathologists to know the

complete structure of the network at risk. One of these is the
immunization of a small fraction of random acquaintances of
randomly selected individuals (acquaintance immunization).
As hubs have by definition a large number of links, the prob-
ability that a random neighbour of a random node is a hub is
very large. This is thus a simple way to identify and remove
highly connected individuals even without knowing who
they are in advance (Cohen et al., 2003; Holme, 2004; Madar
et al., 2004; May, 2006).
Alternatively, ring vaccination of individuals at less than a
certain radius from infected cases has been modelled (e.g.
Ahmed et al., 2002; Pourbohloul et al., 2005), which is both
more effective and more costly the larger the radius chosen
(Dybiec et al., 2004). This is essentially a local strategy and
has long been studied for regular lattices and carried out in
homogenous pathosystems. The same authors report that the
effect of including long-distance interactions in models
(thus moving from a regular network to a small-world one) is
that the radius of the local control strategy has to be greatly
increased, with proportionally poorer cost-effectiveness.
Similar implications for disease control are obtained from
models aiming to determine the best strategy for protecting
computer networks. In this case, of course, the finding that
random removal of links does not affect a scale-free network
is a good rather than a bad thing because it makes networks
more robust (e.g. Vázquez & Moreno, 2003). Similarly, in
computer networks highly connected individuals are not to be
removed to prevent disease spread, but protected to decrease
network vulnerability (e.g. Crucitti et al., 2003). This is because,
in networks with a heterogeneous distribution of connections,
when highly connected individuals are disconnected a global
cascade of failures is likely to follow (e.g. Moreno et al., 2002a;
Motter, 2004; Zhao et al., 2004). Further examples of this
kind include studies of the structural vulnerability of electric
power grids, which were found to be robust to most random
perturbations, but very sensitive to disturbances affecting key
power stations (e.g. Albert et al., 2004; Crucitti et al., 2004;
Chassin & Posse, 2005; Kinney et al., 2005). Similar conclu-
sions about the general robustness of scale-free networks to
random disruptions of their components have been drawn
from studies of metabolic networks (e.g. Albert et al., 2000;
Dorogovtsev & Mendes, 2002), although for plant cells the
picture may be more complicated (Sweetlove & Fernie, 2005).
Case Studies
Not only has the impact of network structure on disease
development been modelled, but the tools of network theory
have been applied to a number of case studies. In this section,
we review some recent empirical applications, drawing
conclusions for epidemiology whenever possible.
An exemplary application of network theory to an epide-
miologic case study is the investigation of how computer
network structure affects so-called epidemic algorithms. These
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Research review Review 285
are mechanisms that allow data dissemination (e.g. software
updates, peer-to-peer networks and database maintenance) to
computers connected in a network (e.g. Acosta-Elias et al.,
2004). Large-scale numerical simulations of epidemic algo-
rithms suggest that in scale-free networks data transfer is more
efficient but less reliable than in homogenous topologies
(Moreno et al., 2004). This finding corroborates the higher
speed of disease spread in scale-free networks pointed out in
the section ‘Disease spread in network’. The lower reliability
emphasizes that disease development in scale-free networks is
stochastically affected by the number of connections of the
first individuals infected (e.g. Keeling, 1999; Verdasca et al.,
2005).
A similar suite of studies is related to the spread of memes
through social networks. By analogy with the susceptible/
infected/removed (SIR) model in epidemiology, individuals
of a population can be subdivided into those not having heard
an idea yet; those aware of the concept and communicating
it to others; and those having become uninterested and not
disseminating it any longer (e.g. Zanette, 2002). Also in this
case, models show that one strategy for a successful dissemi-
nation of memes is to target hubs (e.g. Duan et al., 2005).
Translated into terms of disease control, this finding suggests
again that disease spread can best be constrained in scale-free
networks by removing from the network individuals with the
highest number of connections. For plant diseases that are
spread through the nursery trade, the susceptible/infected/
susceptible (SIS) model may be more realistic, as infected
nurseries, unless under complete quarantine, may continue to
operate even if under surveillance or if plants within a certain
distance from the infected material are quarantined. The
implications of such models will be addressed in the last section
of the review. It is already clear, however, that there are many
examples of spatially structured host–pathogen systems where
the identification of highly connected nodes in the network
underlying the long-distance spread of disease might have
been an effective way to delay plant disease expansion (e.g.
chestnut blight, Dutch elm disease, black sigatoka of banana
and potato blight).
The spread of viruses via email messages in computer
networks is a further instance that has been analysed from a
network theory perspective. A remarkable finding of some
models is that the whole network of computers can be made
immune from infection by the targeted immunization of a
selected 10% of connected computers (Newman et al., 2002).
But further analyses have shown that the way in which a virus
replicates itself can affect the topology of the computer network,
thus making it difficult to control an epidemic (Balthrop et al.,
2004). In this case, epidemic control is also made difficult by
the increasing disparity between the speed of automated dis-
ease spread and that of manual eradication.
Apart from epidemic algorithms and the spread of ideas
and of computer viruses, work applying network theory to
empirical cases can be subdivided into that pertaining to
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286 Review Research review
human and animal diseases. Few applications have referred
to plant diseases.
Network theory applied to human diseases
A whole series of case studies involves human pathologies.
Here the motivation is the greater threat posed by human
pathogens in a more and more interconnected world (e.g.
Eubank et al., 2004; Hufnagel et al., 2004; Brockmann et al.,
2006; Colizza et al., 2006b; Tatem et al., 2006). Recent studies
have been motivated by the threat of pandemic influenza.
Detailed network models of this and of other globally relevant
infectious diseases need accurate estimation of model para-
meters (Ferguson et al., 2005; Longini et al., 2005; Arino
et al., 2006; Colizza et al., 2006a; Germann et al., 2006).
However, for the recent severe acute respiratory syndrome
(SARS) outbreak, modellers found that random networks did
not satisfactorily catch the observed dynamics of the epidemic,
and that only the addition of small-world properties allowed
realistic description of disease development. In particular,
small-world networks are able to account for the otherwise
puzzling disparities between the markedly different develop-
ments of outbreaks that started simultaneously in different
regions (e.g. Masuda et al., 2004; Small et al., 2004, 2006;
Bauch et al., 2005; Meyers et al., 2005). Incorporating the
heterogeneity in the contact structure into models also allows
an accurate matching of predictions with observed dynamics
at relatively small scales, as shown by an analysis of a dengue
outbreak on Easter Island (Favier et al., 2005).
A study of childhood infections dynamics in Canada
showed that it is possible to reconstruct the probable network
structure for a disease given the time-series data of the epi-
demics. The epidemic size distribution follows an inverse
power-law for rubella and mumps, implying heterogeneous
individual contacts and thus a scale-free network; whereas for
pertussis a homogenous transmission network is suggested by
the exponential distribution of epidemic sizes (Trottier &
Philippe, 2005). When the basic structure of a network is
known, as in the case of an outbreak of bacterial pneumonia
in a residential institution where a household structure was
clearly present in the different wards, models can help the
management of the disease by pointing out that nurses are the
super-spreaders who need to be immunized (Meyers et al.,
2003). A similar result, showing that preventive measures
need to be applied to individuals with many partners, was
found in analyses of an outbreak of gonorrhoea in Alberta,
Canada (De et al., 2004).
The last example is part of the research using network
theory to improve forecasts of the spread of sexually transmitted
diseases (STDs; e.g. Liljeros et al., 2001, 2003; Eames &
Keeling, 2002; Jolly et al., 2005). Modelling work on STDs
illustrates that for real populations of finite size, even though
organized in a scale-free network, there exists a non-null
epidemic threshold, so the spread of STDs can be stopped
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(Gonçalves & Kuperman, 2003; Jones & Handcock, 2003).
Whether the dynamic nature (sexual partnerships may evolve
through time) of these networks will tend to facilitate (by
creating new connections) or hamper (by disrupting the
structure of the network) the spread of STDs deserves further
investigation, also in the context of venereal diseases of plants
(Antonovics, 2005). However, sexual partnership networks
tend to be scale-free, as the distribution of the number of
sexual partners cumulated over time typically follows an
inverse power-law. In this case, only targeted action (aimed at
individuals connecting subgroups of the population) can be
effective in preventing further spread of STDs (e.g. Liljeros,
2004; Schneeberger et al., 2004). An example is the use of
network data to predict the development of an AIDS out-
break in Houston, Texas, USA, where data on social network
structure were assessed as the most important requirement for
more effective management (Bell et al., 2002).
Network theory applied to animal diseases
A prime example of the application of network analysis to the
study of disease spread in animals is foot and mouth disease
(FMD). Much modelling work has been done following the
2001 outbreak in the UK (e.g. Woolhouse, 2003; Keeling,
2005a). But in this case too, it has been advocated that models
need to use aspects of network theory (e.g. Haydon et al.,
2003; Shirley & Rushton, 2005b; Woolhouse et al., 2005).
This is because of the long-distance dispersal exhibited by the
viral pathogen (via farm management, commercial exchanges,
and possibly airborne dispersal), and by the scale-free contact
structure of the farm network, including hubs such as markets
and animal shows (e.g. Keeling et al., 2003; Shirley &
Rushton, 2005b; Webb, 2005, 2006; Kiss et al., 2006b).
However, Woolhouse et al. (2005) argue that, even if the
network among livestock farms has a scale-free distribution of
contacts, the basic reproduction number is not increased by
this because the probability of one farm infecting another was
not significantly related to the probability of the first farm
becoming infected itself.
For the FMD outbreak of 2001 in the UK, a reconstruction
of epidemic trees (from putative sources of infection for
infected premises) revealed that, if the national ban on move-
ment of cattle had been declared 2 d earlier, the size of the
epidemic would probably have been reduced by half (Haydon
et al., 2003). Even more effective would have been the removal
from the network of the three hubs from which nearly 80%
of subsequent infections are thought to have originated.
Unfortunately, livestock can spread the disease without show-
ing clinical signs of it for up to 10 d (Shirley & Rushton,
2005b), so the rapid identification of the markets that caused
the long-range spread of the disease was not possible.
FMD is only one example of the many wildlife diseases
potentially spread by movements of animals (Woolhouse
et al., 2005). Network analyses related to wildlife diseases

include a study of bovine tuberculosis of African buffalo in
Kruger National Park, South Africa (Cross et al., 2004). This
showed that buffalo herds were less tightly clustered in years
of dry weather, and that this mixing of the overall population
could lead to faster spread of the disease. A somewhat different
example is an assessment of the role of long-distance dispersal
for the spread of raccoon rabies in Connecticut, USA (Smith
et al., 2005). In this case, establishment of disease foci from
small-world shortcuts was rare, and the disease can be man-
aged with a local containment strategy. A different finding in
relation to Lyme disease is that in northern Spain there are
critical stepping-stone habitats with high tick densities, whose
removal can markedly alter the connectivity of the landscape
(Estrada-Peña, 2003).
Network theory applied to plant diseases
The applications of network theory discussed above prompt
the question of whether network theory can also improve our
understanding of the spread of plant and tree diseases. Of
course, plants are not as mobile as humans and animals
(although their pathogens are not static, and plants themselves
can cross long distances from one generation to the next
through seeds, pollen and, in some cases, vegetative material).
In fact, at a first glance plants do not seem to form social scale-
free networks of highly mobile interactions such as, for instance,
fish are classically able to materialize, thus potentially facilitating
the spread of their epidemics (e.g. Croft et al., 2004, 2005).
This may explain why there has so far been relatively little
use of network theory in plant epidemiology. Models of
epidemics on networks, rather than in continuous space or
on lattices, might work better for animal or human than for
plant diseases (Bolker, 1999). But there exist threads of plant
epidemiological research that use meta-population theory,
and in many cases follow similar lines of reasoning to
modelling work on networks (e.g. Hanski, 1994; Park et al.,
2001, 2002; Gilligan, 2002; Franc, 2004; Otten et al., 2004,
2005; Vuorinen et al., 2004; Watts et al., 2005; Brooks, 2006).
Potential Implications for Plant and Forest
Pathology
Network theory may be relevant to plant diseases, but not
yet have been applied. If so, one explanation of the delayed
application may be that the theory is not yet sufficiently
mathematically developed to apply to epiphytotics, as plant–
pathogen networks in the real world are not only complex,
but transient and dynamic. Another explanation is that
plant epidemiologists need the development of appropriate
software tools to exploit the potential of network theory (see
Garrett et al., 2004). It may also be that data on the network
structure of plant communities are frequently harder to
obtain than the often meticulous records for human and
animal epidemics.
© The Authors (2007). Journal compilation © New Phytologist (2007) www.newphytologist.org
Research review Review 287
But studies are beginning to show that plant communities
can be part of scale-free networks, at least when considered in
conjunction with other interacting species (on their own,
plants seem to depart from a true fractal spatial distribution;
e.g. Lennon et al., 2002; see also Erickson, 1945; Kunin,
1998). An intriguing related question is whether such an
absence of a fractal spatial distribution for plants would pre-
clude the existence of a scale-free network (e.g. Berntson &
Stoll, 1997). For example, a network of plants and their pol-
linator species in Greenland was found to show small-world
properties (Lundgren & Olesen, 2005). High clustering and
small path length between plant species were also reported
from a study of the network of frugivorous birds and fleshy-
fruited plant species in Denmark (Lázaro et al., 2005). These
studies are only a few of many investigations of plant–pollinator
and plant–frugivore networks. However, these webs may not
generally show scale-free properties as, in an analysis of 53
such networks in natural communities, only roughly one-fifth
exhibited scale invariance in the connectivity distribution
(Jordano et al., 2003). The reasons for such a finding are
being debated, but the range of scales involved in each case
may be of relevance here (see also Khanin & Wit, 2006). Myc-
orrhizal networks, when seen from a mycocentric point of
view (i.e. considering individual trees as connecting fungal
morphotypes and not vice versa), can be scale-free (South-
worth et al., 2005). There is much research potential in inves-
tigating whether this scale invariance is present more generally
in microbial, mycelial and host–parasitoid networks (e.g.
Davidson et al., 1996; Klein & Paschke, 2004; Cairney, 2005;
Károlyi, 2005; Killingback et al., 2006; see also Friesen et al.,
2006). Of course, scale-free networks may also be relevant in
plant sciences in relation to food webs (e.g. Dunne et al.,
2002) and from a metabolic point of view (e.g. Sweetlove &
Fernie, 2005; Uhrig, 2006), for instance in the context of the
pathways controlling stomata at different scales (Hetherington
& Woodward, 2003).
Provided that it is feasible to obtain network data from
plant and forest ecosystems, there are a number of reasons to
think that network theory may be a convenient tool when
dealing with the health of plant and forest pathosystems. In a
modern landscape, it may be relatively easy to recognize a scale
of description at which one should switch to a network. For
crop plants, the obvious unit are fields, farms and trading
units on a production chain; for trees, nodes may be forest
stands, plantations, urban parks and tree nurseries. The great
promise of network theory is that it can help in investigating
how disease development parameters vary within and across
individual meta-populations (Heesterbeek & Zadoks, 1987;
Parnell et al., 2006). Moreover, shipments of plants across
continents are a matter of routine nowadays, with often
unpredictable consequences for the introduction and spread
of exotic plants and their pathogens (e.g. Reichard & White,
2001; Stokstad, 2004; Dumroese & James, 2005; Perrings
et al., 2005; Dehnen-Schmutz et al., 2007).
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288 Review Research review
There is thus a need to assess the properties of plant nursery
networks in a number of representative regions and for various
pathogens and endophytes (e.g. Stanosz et al., 2005; Giménez-
Jaime et al., 2006; Menkis et al., 2006; Pinto et al., 2006;
Stepniewska-Jarosz et al., 2006). This need is immediate
wherever nurseries have been tested positive for the presence
of Phytophthora ramorum, the causal agent of sudden oak
death (e.g. Parke et al., 2004; Daughtrey & Benson, 2005;
Rizzo et al., 2005; Fig. 2). Figure 2 suggests that contact tracing
information about ongoing and eradicated outbreaks of
P. ramorum in the UK may enable the reconstruction of the
network underlying the spread of the pathogen, which in turn
might enable a more effective control strategy. Nurseries may
also be contributing to the spread of Phytophthora alni, as a
study from Bavaria suggests ( Jung & Blaschke, 2004), of the
western flower thrips Frankliniella occidentalis, which is the
vector of tospoviruses, both in North America and in Europe
(Kirk & Terry, 2003; Jones et al., 2005), and of Ralstonia
solanacearum, the bacterium causing potato brown rot, which
has been the object of individual-based modelling in the
Netherlands (Breukers et al., 2006). A network approach
seems sensible also in relation to botanical gardens, which
acted historically as hubs in the introduction of plants outside
their natural geographic range (e.g. Mamaev & Andreev,
1996; Ingram, 1999; He, 2002). It remains true that under-
standing the network, especially its topology, is useful in
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Fig. 2 Findings of Phytophthora ramorum on
plants at retail (crosses), nursery (diamonds),
estates/environment (squares) and other
(triangles) sites in England and Wales in
2003–2005. Data source: Department for
Environment, Food and Rural Affairs, UK.
devising effective disease management policies even if there is
probably no single immunization strategy that can be effective
for all types of scale-free networks (Volchenkov et al., 2002).
Network thinking may also be relevant for natural plant
communities because, although individuals cannot move,
seeds can, and provide a means of long-distance dispersal and
invasion for species with appropriate life history traits (e.g.
Grotkopp et al., 2002; Pysek et al., 2004; Richardson &
Rejmanek, 2004; Zedler & Kercher, 2004; Hamilton et al.,
2005). There is evidence that the level of long-distance disper-
sal in tree recolonization after glaciations can determine the
genetic pool of newly founded populations (Le Corre et al.,
1997; Petit et al., 2004; Bialozyt et al., 2006). It could be useful
to describe invasion processes with flows along the network
of locations where a plant species establishes itself; it is
possible that this would reveal differences between fast and
slow invaders. Network theory might be combined with
landscape genetics to improve our understanding of the con-
sequences of rapid climate change, as now predicted, for plant
(and associated pathogen) distributions (e.g. Manel et al.,
2003; Bacles et al., 2004; Neilson et al., 2005; Simberloff
et al., 2005; Webber & Brasier, 2005).
Although contact tracing of disease is often impractical
both in plantations and in more pristine forests, recent studies
demonstrate that it is possible to track long-range spore dis-
persal of wood-decaying fungal organisms (e.g. Edman et al.,

2004). Will this enable the reconstruction of the colonization
history of these endangered species, so as to allow a rough
understanding of the type of network involved? It is known
that models predicting travelling waves of pathogen spread
at constant speed are unrealistic if spore dispersal of plant
pathogens is best fitted by a fat-tailed and not an exponential
distribution (e.g. Ferrandino, 1993; Shaw, 1995; see also
Scherm, 1996; Gibson, 1997; Jeger, 1999; Brown & Hovmøller,
2002; Bicout & Sache, 2003; Filipe & Maule, 2004; Shaw
et al., 2006). This issue is also relevant for investigations of the
effect of landscape structure on the spread of P. ramorum in
California (e.g. Meentemeyer et al., 2004; Rizzo et al., 2005).
In the landscape of forest and grassland patches where the
pathogen is currently spreading, dispersal gradients will be
affected by relatively efficient impaction and slow wind speeds
within forest patches but by inefficient deposition and faster
winds through open areas, with potentially different spore
dispersal functions in the two cases.
Insect vectors are another way for fungal pathogens of
plants to jump from patch to patch of potential hosts in a
landscape without other dispersal pathways (e.g. Geils, 1992).
Elm bark beetles (Coleoptera: Scolytidae), the vectors of Dutch
elm disease, attack clusters of debilitated trees, and in many
cases avoid local dispersal to neighbouring healthy trees by fly-
ing long distances to different forest patches. There is evidence
that the presence of elm trees (Ulmus spp.) in the landscape is
made more manifest to elm bark beetles by sesquiterpene
emissions induced on infected trees by the fungus responsible
for Dutch elm disease (McLeod et al., 2005). This implies that
the underlying network structure of the pathosystem is dynamic,
and can differ from that deduced from the distribution of trees
in the landscape. In the case of infections spread by vectors,
managers may profitably make use of models incorporating mobile
agents in the study of disease spread in complex networks
(e.g. Miramontes & Luque, 2002; González & Herrmann,
2004; Frasca et al., 2006; see also Rvachev & Longini, 1985).
Network modelling including mobile agents may, for instance,
help in understanding and predicting the progress of inva-
sions such as that of the horse chestnut leaf miner, Cameraria
ohridella, which is facilitated by car movements and therefore
follows major roads (e.g. Gilbert et al., 2005). Other potential
applications of network theory in plant and forest pathology
include the spread of fire blight (Erwinia amylovora; e.g. Jock
et al., 2002) and of chestnut blight (Cryphonectria parasitica)
hypovirulence (e.g. Milgroom & Cortesi, 2004).
A network description of a tree pathosystem from a phyto-
centric point of view would specify nodes (host trees) and the
links between them by whatever transport mechanism is
responsible for spreading the disease, with or without any
explicit geography. If data were available at a sufficiently large
scale, it would be interesting to compare the networks of the
population structure of newly introduced, aggressive tree
pathogens (e.g. Phytophthora cinnamomi; e.g. Hardham, 2005)
with those of endemic, long established ones (e.g. Heteroba-
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Research review Review 289
sidion annosum s.l.; e.g. Asiegbu et al., 2005). Unfortunately,
to the best of our knowledge, only data from the local foraging
behaviour of pathogens are available (for e.g. Armillaria spp.;
Prospero et al., 2003a,b; Mihail & Bruhn, 2005), although
large-scale information is accumulating, for example for the
tree root endophyte and opportunistic pathogen Phialocephala
fortinii s.l. (e.g. Queloz et al., 2005; Grünig et al., 2006). Net-
work models might help in predicting the outcome of the
dynamic interactions between pathogens of tree stumps and
saprotrophic fungi used as biological control agents (Holden-
rieder & Greig, 1998; Boddy, 2000). Models suggest that by
manipulating the network structure it may be possible to
diminish the incidence of one of two competing species, to
the benefit of the other (Newman, 2005b). But other model-
ling work on the spread of two social norms in a network
suggests that the contact structure may not be the only factor
determining the outcome of the interactions between two
competing species (Nakamaru & Levin, 2004).
Heterogeneous forested landscapes are hard to represent as
regular grids and contain multiple layers of evolving interactions.
Elaborations of basic models of disease spread in networks
may allow us to use insights provided by network theory in
these ecosystems. Models making use of small-world net-
works in the simulation of the spread of forest fires are already
established (e.g. Moukarzel, 1999; Graham & Matthai, 2003;
Porterie et al., 2005) and have much more potential. It would
be most fascinating to use these models to integrate the
combined effects of sudden oak death and fire (Moritz &
Odion, 2005). The patchiness of the host distribution and of
environmental conditions may contribute to the heterogene-
ous spread of epidemics in forests (e.g. Sander et al., 2003;
Vannucchi & Boccaletti, 2004). Models trying to include in
their structure the variable susceptibility of hosts have cer-
tainly much scope for application in real forests (e.g. Sander
et al., 2002). Models investigating the effect of the contact
structure of networks on pathogen diversity (e.g. Buckee
et al., 2004; Nunes et al., 2006) also offer new insights and
possibly practical applications. Given the often long time-
scale of disease evolution in real forests, models can provide a
rapid forecast of the direction towards which a pathosystem
may evolve, given a certain network structure (e.g. Read &
Keeling, 2003; Ferrari et al., 2006; Kao, 2006). A network
perspective can also help in the selection of protected areas,
because of the importance for the success of conservation
efforts of understanding the connectivity within meta-
populations (e.g. Brito & Grelle, 2004; Frank, 2004; Cerdeira
et al., 2005).
Conclusion
Network theory will be a useful addition to the set of concepts
and tools available to understand and manage disease in plant
populations. It may have its most obvious uses, as in our
examples, in human-modified pathosystems where discrete,
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290 Review Research review
separated units can be identified, and where commercial
transport may make distance a poor guide to the strength of
a link between two units. It is less likely to be useful where
the capacity of channels depends simply on proximity, and
homogeneity is a reasonable approximation to the plant spatial
distribution. But given the interconnectedness of today’s
world, it may matter less and less that the long-distance jumps
characteristic of wind-blown pathogens are hard to describe in
a network model. The key factor in an increasing number of
epiphytotics today is the transport by humans of disease
propagules. Anything involving human transport of plants or
their pathogens may be usefully modelled as a network, at
least at some stage. We argue that more use of network theory
in plant epidemiology would ensure that the critical features
of many real epidemics would be clarified and studied earlier
than if the normal task is regarded as modelling dispersal
on a grid or even growth in a homogeneous population.
Modelling work arising from issues in plant epidemiology
may also motivate the investigation of questions of basic
mathematical interest.
Acknowledgements
Many thanks to A. Ramsay, N. Russell and R. Smith for
comments on a previous version of this draft and to R. Baker,
S. Hardy, T. Harwood, A. Inman, N. Künzli, J. Parke, L. Paul,
V. Queloz, N. Salama, C. Sansford, T. Sieber, P. Todeschini,
J. Webber and X. Xu for insights and discussions. The com-
ments of two anonymous reviewers were particularly helpful.
Work on this review was funded by the Department for
Environment, Food and Rural Affairs, UK and is partly based
on a talk on Epidemiology and Networks at the APS, CPS &
MSA joint meeting in Quebec City, July 2006.
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