Emergence of new leptospiral serovars in American Samoa - ascertainment or ecological change?
1 School of Population Health, The University of Queensland, Herston, Queensland, 4006, Australia
2 WHO/OIE/FAO Collaborating Centre for Reference and Research on Leptospirosis, Queensland Health Forensic and Scientific Services, Coopers Plains, Queensland 4108, Australia
3 Faculty of Science, Health and Education, University of the Sunshine Coast, Sippy Downs, Queensland 4556, Australia
4 Barbara Hardy Institute, University of South Australia, Adelaide, South Australia 5001, Australia
BMC Infectious Diseases 2012, 12:19 doi:10.1186/1471-2334-12-19Published: 25 January 2012
Leptospirosis has recently been discussed as an emerging infectious disease in many contexts, including changes in environmental drivers of disease transmission and the emergence of serovars. In this paper, we report the epidemiology of leptospiral serovars from our study of human leptospirosis in American Samoa in 2010, present evidence of recent serovar emergence, and discuss the potential epidemiological and ecological implications of our findings.
Serovar epidemiology from our leptospirosis seroprevalence study in 2010 was compared to findings from a study in 2004. The variation in geographic distribution of the three most common serovars was explored by mapping sero-positive participants to their place of residence using geographic information systems. The relationship between serovar distribution and ecological zones was examined using geo-referenced data on vegetation type and population distribution.
Human leptospirosis seroprevalence in American Samoa was 15.5% in 2010, with serological evidence that infection was caused by three predominant serovars (Hebdomadis, LT 751, and LT 1163). These serovars differed from those identified in an earlier study in 2004, and were not previously known to occur in American Samoa. In 2010, serovars also differed in geographic distribution, with variations in seroprevalence between islands and different ecological zones within the main island.
Our findings might indicate artefactual emergence (where serovars were long established but previously undetected), but we believe the evidence is more in favour of true emergence (a result of ecological change). Possibilities include changes in interactions between humans and the environment; introduction of serovars through transport of animals; evolution in distribution and/or abundance of animal reservoirs; and environmental changes that favour transmission of particular serovars.
Future research should explore the impact of ecological change on leptospirosis transmission dynamics and serovar emergence, and investigate how such new knowledge might better target environmental monitoring for disease control at a public health level.