Effects of heterogeneous and clustered contact patterns on infectious disease dynamics

The spread of infectious diseases fundamentally depends on the pattern of contacts between individuals. Although studies of contact networks have shown that heterogeneity in the number of contacts and the duration of contacts can have far-reaching epidemiological consequences, models often assume that contacts are chosen at random and thereby ignore the sociological, temporal and/or spatial clustering of contacts. Here we investigate the simultaneous effects of heterogeneous and clustered contact patterns on epidemic dynamics. To model population structure, we generalize the configuration model which has a tunable degree distribution (number of contacts per node) and level of clustering (number of three cliques). To model epidemic dynamics for this class of random graph, we derive a tractable, low-dimensional system of ordinary differential equations that accounts for the effects of network structure on the course of the epidemic. We find that the interaction between clustering and the degree distribution is complex. Clustering always slows an epidemic, but simultaneously increasing clustering and the variance of the degree distribution can increase final epidemic size. We also show that bond percolation-based approximations can be highly biased if one incorrectly assumes that infectious periods are homogeneous, and the magnitude of this bias increases with the amount of clustering in the network. We apply this approach to model the high clustering of contacts within households, using contact parameters estimated from survey data of social interactions, and we identify conditions under which network models that do not account for household structure will be biased.     

Detrimental effects of environmental tobacco smoke in relation to asthma severity

Background

Environmental tobacco smoke (ETS) has adverse effects on the health of asthmatics, however the harmful consequences of ETS in relation to asthma severity are unknown.

Methods

In a multicenter study of severe asthma, we assessed the impact of ETS exposure on morbidity, health care utilization and lung functions; and activity of systemic superoxide dismutase (SOD), a potential oxidative target of ETS that is negatively associated with asthma severity.

Findings

From 2002–2006, 654 asthmatics (non-severe 366, severe 288) were enrolled, among whom 109 non-severe and 67 severe asthmatics were routinely exposed to ETS as ascertained by history and validated by urine cotinine levels. ETS-exposure was associated with lower quality of life scores; greater rescue inhaler use; lower lung function; greater bronchodilator responsiveness; and greater risk for emergency room visits, hospitalization and intensive care unit admission. ETS-exposure was associated with lower levels of serum SOD activity, particularly in asthmatic women of African heritage.

Interpretation

ETS-exposure of asthmatic individuals is associated with worse lung function, higher acuity of exacerbations, more health care utilization, and greater bronchial hyperreactivity. The association of diminished systemic SOD activity to ETS exposure provides for the first time a specific oxidant mechanism by which ETS may adversely affect patients with asthma.     

Growth and multiplication ofRhodotorula glutinis as determined by viable and total cell counts

Excellent correlation has been shown between two total and two culture, or viable, count techniques used for cell enumeration studies ofRhodotorula glutinis. The culture methods examined, the drop plate and the spread plate proved equally reliable for enumeration except for slight variations during the period of maximal budding of the organism. The Coulter Counter was a valuable tool as it permitted rapid cell population analysis with minimal preparatory procedures. The Petroff-Hausser counting chamber was found applicable only when cell numbers approached 10⁹ or greater.Contribution No. 468 from the Marine Laboratory, Institute of Marine Science, University of Miami, Miami, Florida, U.S.A. Supported by Grant G-16146 from the National Science Foundation.     

Anatomy and histochemistry of spread-wing posture in birds. 3. Immunohistochemistry of flight muscles and the "shoulder lock" in albatrosses

As a postural behavior, gliding and soaring flight in birds requires less energy than flapping flight. Slow tonic and slow twitch muscle fibers are specialized for sustained contraction with high fatigue resistance and are typically found in muscles associated with posture. Albatrosses are the elite of avian gliders; as such, we wanted to learn how their musculoskeletal system enables them to maintain spread-wing posture for prolonged gliding bouts. We used dissection and immunohistochemistry to evaluate muscle function for gliding flight in Laysan and Black-footed albatrosses. Albatrosses possess a locking mechanism at the shoulder composed of a tendinous sheet that extends from origin to insertion throughout the length of the deep layer of the pectoralis muscle. This fascial "strut" passively maintains horizontal wing orientation during gliding and soaring flight. A number of muscles, which likely facilitate gliding posture, are composed exclusively of slow fibers. These include Mm. coracobrachialis cranialis, extensor metacarpi radialis dorsalis, and deep pectoralis. In addition, a number of other muscles, including triceps scapularis, triceps humeralis, supracoracoideus, and extensor metacarpi radialis ventralis, were found to have populations of slow fibers. We believe that this extensive suite of uniformly slow muscles is associated with sustained gliding and is unique to birds that glide and soar for extended periods. These findings suggest that albatrosses utilize a combination of slow muscle fibers and a rigid limiting tendon for maintaining a prolonged, gliding posture.     

Network theory and SARS: predicting outbreak diversity

Many infectious diseases spread through populations via the networks formed by physical contacts among individuals. The patterns of these contacts tend to be highly heterogeneous. Traditional "compartmental" modeling in epidemiology, however, assumes that population groups are fully mixed, that is, every individual has an equal chance of spreading the disease to every other. Applications of compartmental models to Severe Acute Respiratory Syndrome (SARS) resulted in estimates of the fundamental quantity called the basic reproductive number R0--the number of new cases of SARS resulting from a single initial case--above one, implying that, without public health intervention, most outbreaks should spark large-scale epidemics. Here we compare these predictions to the early epidemiology of SARS. We apply the methods of contact network epidemiology to illustrate that for a single value of R0, any two outbreaks, even in the same setting, may have very different epidemiological outcomes. We offer quantitative insight into the heterogeneity of SARS outbreaks worldwide, and illustrate the utility of this approach for assessing public health strategies.