K - College of Natural Resources - University of California, Berkeley

equired for the derivation means that pair-based STD transmission is portrayed accurately only
for promiscuous populations and chronic, less-transmissible infections. Simulations define the
limits of the classical model for two broad classes of STD. I then extend the derivation to
include situations where infected individuals exhibit altered pairing behavior, presenting
analytic expressions for the generalized frequency-dependent transmission rate, basic
reproductive number (R0), and steady-state prevalence of an epidemic, for four cases of
increasing behavioral complexity. Potentially significant effects of infection-induced changes
in contact behavior are illustrated by simulating epidemics of bacterial and viral STDs.
In Chapter 3, I investigate the stochastic invasion dynamics of an emerging disease in a
community and its associated hospital, exploring for the first time the potential amplifying role
of hospitals in an outbreak characterized by nosocomial spread. Severe acute respiratory
syndrome (SARS) was transmitted extensively within hospitals, and healthcare workers
comprised a large proportion of SARS cases worldwide. I evaluate contact precautions and
case management (quarantine and isolation) as control measures for SARS, revealing that
hospital infection control is the most potent measure and should be practiced by all individuals
in affected hospitals, rather than only those interacting with known SARS cases. Delays of a
few days in contact tracing and case identification severely degrade the utility of quarantine and
isolation, and still more detrimental are delays between onset of an outbreak and
implementation of control measures. If hospital-based transmission is not halted, measures
which reduce community-healthcare worker contact are vital to preventing a widespread
epidemic. These results have implications for future outbreaks of SARS or other emerging
pathogens.
In Chapter 4, I address the impact of individual-level variation in infectiousness, and
resulting superspreading events (SSEs), on disease emergence. I introduce the “individual
reproductive number”, a natural extension of the basic reproductive number R0 from a
population average to a distribution incorporating individual variation. The degree of individual
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