Abstract A large number of infectious diseases are believed to be transmitted between people via large droplets and by airborne routes. An understanding of evaporation and dispersion of droplets and droplet nuclei is not only significant for developing effective engineering control methods for infectious diseases but also for exploring the basic transmission mechanisms of the infectious diseases. How far droplets can move is related to how far droplet-borne diseases can transmit. A simple physical model is developed and used here to investigate the evaporation and movement of droplets expelled during respiratory activities; in particular, the well-known Wells evaporation–falling curve of droplets is revisited considering the effect of relative humidity, air speed, and respiratory jets. Our simple model considers the movement of exhaled air, as well as the evaporation and movement of a single droplet. Exhaled air is treated as a steady-state non-isothermal (warm) jet horizontally issuing into stagnant surrounding air. A droplet is assumed to evaporate and move in this non-isothermal jet. Calculations are performed for both pure water droplets and droplets of sodium chloride (physiological saline) solution (0.9% w/v). We calculate the droplet lifetimes and how droplet size changes, as well as how far the droplets travel in different relative humidities. Our results indicate that a droplet's size predominately dictates its evaporation and movement after being expelled. The sizes of the largest droplets that would totally evaporate before falling 2 m away are determined under different conditions. The maximum horizontal distances that droplets can reach during different respiratory activities are also obtained. Our study is useful for developing effective prevention measures for controlling infectious diseases in hospitals and in the community at large.

Information on the clinical features of the severe acute respiratory syndrome (SARS) will be of value to physicians caring for patients suspected of having this disorder.

Paradoxical deterioration during antituberculosis therapy, defined as the clinical or radiological worsening of pre-existing tuberculous lesions or the development of new lesions in a patient who initially improves, remains a diagnostic dilemma. Although different clinical presentations of paradoxical response have been described, a systematic analysis of the entity in non-HIV-infected patients is lacking. Reported here are two cases of paradoxical deterioration in which sequential changes in lymphocyte counts and tuberculin skin test results are emphasized. In addition, 120 episodes of paradoxical response after antituberculosis treatment were reviewed. Of the total 122 episodes, 101 (82.8%) were associated with extrapulmonary tuberculosis. The median time from commencement of treatment to paradoxical deterioration was 60 days. The median time to onset of central nervous system manifestations (63 days) was longer than the time to onset of manifestations at other sites (56 days) (P=0.02). Development of new lesions in anatomical sites other than those observed at initial presentation was observed in 31 (25.4%) episodes. A surge in the lymphocyte count, accompanied by an exaggerated tuberculin skin reaction, was observed in our patients during the paradoxical deterioration, analogous to the findings in HIV-positive patients. Treatment of the paradoxical response included surgical intervention (60.7%) and administration of steroids (39.3%). The use of steroids appeared to be safe in this series, as 95% of the Mycobacterium tuberculosis isolates were susceptible to first-line antituberculosis therapy.