Cattle may spread leptospirosis in Africa, study suggestsJune 07, 2018
The bacterial infection leptospirosis is increasingly recognized as an important cause of fever in Africa. Now, researchers reporting in PLOS Neglected Tropical Diseases have analyzed the major risk factors for contracting leptospirosis and discovered that rice and cattle farming are associated with acute infection.
Leptospirosis, caused by bacteria of the genus Leptospira, causes a wide range of symptoms and can lead to serious complications include kidney and liver problems. In one study conducted in northern Tanzania, 8.8% of people with severe fevers had leptospirosis. Scientists know that animals can carry leptospirosis and lead to its spread throughout the environment or directly to humans. However, the major animal reservoirs and modes of transmission have not been well described.
In the new work, Michael Maze of the University of Otago, New Zealand, and colleagues enrolled people with fever from two hospitals in Moshi, Tanzania from 2012 through 2014. Each participant was tested for leptospirosis, and administered a survey on risk behaviors over the past 30 days, including exposure to livestock, rodents, and surface water.
The researchers identified 24 acute cases of leptospirosis, 252 people positive for lower levels of Leptospira bacteria (seropositivity), and 592 controls. Rice farming, cleaning cattle waste, feeding cattle and farm work were all positively associated with acute leptospirosis. Smallholder farming-- which may be associated with substantial exposure to both livestock and rodents--as well as frequent sightings of rodents in one's kitchen or food store-- was associated with seropositivity.
"Our findings suggest that control of Leptospira infection in livestock could play a role in preventing human leptospirosis in Africa," the researchers say.
Citation: Maze MJ, Cash-Goldwasser S, Rubach MP, Biggs HM, Galloway RL, et al. (2018) Risk factors for human acute leptospirosis in northern Tanzania. PLOS Neglected Tropical Diseases 12(6): e0006372.https://doi.org/10.1371/journal.pntd.0006372
Funding: This work was supported by the joint US National Institutes of Health (NIH:http://www.nih.gov)-National Science Foundation (NSF:http://www.nsf.gov) Ecology of Infectious Disease program (R01TW009237) and the Research Councils UK, Department for International Development (UK) and UK Biotechnology and Biological Sciences Research Council (BBSRC:http://www.bbsrc.ac.uk) (grant numbers BB/J010367/1, BB/L018926, BB/L017679, BB/L018845), and in part by an US National Institutes of Health International Studies on AIDS Associated Co-infections (ISAAC) award (grant number U01 AI062563) and in part by the Bill & Melinda Gates Foundation funded Typhoid Fever Surveillance in sub-Saharan Africa Program (TSAP) grant (grant number OPPGH5231).
Michael Maze received support from University of Otago scholarships: the Frances G. Cotter Scholarship and the MacGibbon Travel Fellowship. Shama Cash-Goldwasser and Matthew P. Rubach received support from National Institutes of Health Research Training Grants (grant numbers R25 TW009337 and R25 TW009343) funded by the Fogarty International Center and the National Institute of Mental Health. Holly M. Biggs received support from the National Institutes of Health Interdisciplinary Research Training Program in AIDS (grant number NIAID-AI007392). Katrina J. Allan received support from the Wellcome Trust (http://www.wellcome.ac.uk) (grantnumber 096400/Z/11/Z). Matthew P. Rubach, Venance P. Maro, Charles Muiruri, and John A. Crump received support from a US National Institutes of Health National Institute for Allergy and Infectious grant (grant number R01 AI121378). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interests: The authors have declared that no competing interests exist.
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