Superspreading and the effect of individual variation on disease emergence.

Population-level analyses often use average quantities to describe heterogeneous systems, particularly when variation does not arise from identifiable groups. A prominent example, central to our current understanding of epidemic spread, is the basic reproductive number, R(0), which is defined as the mean number of infections caused by an infected individual in a susceptible population. Population estimates of R(0) can obscure considerable individual variation in infectiousness, as highlighted during the global emergence of severe acute respiratory syndrome (SARS) by numerous 'superspreading events' in which certain individuals infected unusually large numbers of secondary cases. For diseases transmitted by non-sexual direct contacts, such as SARS or smallpox, individual variation is difficult to measure empirically, and thus its importance for outbreak dynamics has been unclear. Here we present an integrated theoretical and statistical analysis of the influence of individual variation in infectiousness on disease emergence. Using contact tracing data from eight directly transmitted diseases, we show that the distribution of individual infectiousness around R(0) is often highly skewed. Model predictions accounting for this variation differ sharply from average-based approaches, with disease extinction more likely and outbreaks rarer but more explosive. Using these models, we explore implications for outbreak control, showing that individual-specific control measures outperform population-wide measures. Moreover, the dramatic improvements achieved through targeted control policies emphasize the need to identify predictive correlates of higher infectiousness. Our findings indicate that superspreading is a normal feature of disease spread, and to frame ongoing discussion we propose a rigorous definition for superspreading events and a method to predict their frequency.

Ticarcillin plus clavulanic acid versus moxalactam therapy of osteomyelitis, septic arthritis, and skin and soft tissue infections.

A controlled, randomized study to compare the efficacy and safety of ticarcillin plus clavulanic acid with moxalactam was carried out in 25 evaluable patients with bone, joint, and skin or skin structure infections. Of the 13 patients in the ticarcillin plus clavulanic acid-treated group, nine had osteomyelitis, two had septic arthritis, one had cellulitis, and one had a wound infection. Four of the 12 moxalactam-treated patients had osteomyelitis, one had septic arthritis, and the other seven had cellulitis and/or infected ulcers. A total of 21 causative organisms were isolated in the group treated with ticarcillin plus clavulanic acid: Enterobacteriaceae (10), Pseudomonas aeruginosa (five), obligate anaerobes (three), Staphylococcus aureus (two), and Acinetobacter species (one). Cultures in the moxalactam-treated group yielded 23 pathogens: Enterobacteriaceae (seven), S. aureus (six), group B streptococci (four), P. aeruginosa (two), obligate anaerobes (two), Streptococcus pyogenes (one), and Aeromonas species (one). A cure or satisfactory response was achieved in 12 of the 13 (92 percent) patients who received ticarcillin plus clavulanic acid and in 10 of the 12 (83 percent) patients who received moxalactam. One patient with septic arthritis who received ticarcillin plus clavulanic acid had a relapse during therapy, as did one moxalactam-treated patient with a post-surgical wound infection. The other patient in whom moxalactam treatment failed had a wound infection that became reinfected. Some abnormalities in laboratory parameters occurred in each group, but none was severe enough to warrant discontinuation of treatment.

Primary meningococcal arthritis.

We have reported a case of primary meningococcal arthritis of the left ankle in a previously healthy man. Although primary meningococcal arthritis clinically resembles gonococcal arthritis, prolonged antibiotic therapy and open joint drainage are often required. Even with prompt appropriate antibiotic and surgical therapy, primary meningococcal arthritis may lead to permanent joint damage.