Pathogen Flow: What We Need to Know

We are in the midst of a global health crisis involving the spread of drug-resistant strains of a wide range of microorganisms [Levy & Marshall, 2004]. The evolution of resistance is driven by inappropriate prescription of antimicrobial drugs, the widespread use of antibiotics in agriculture, and failure by patients to complete courses of prescribed antibiotics. One recent study, for example, estimated that 94,360 cases of invasive methicillin-resistant Staphylococcus aureus occurred in the United States in 2005, resulting in 18,650 deaths [Klevens et al., 2007]. Additional research has uncovered a resistance “hotspot” for the protozoa that cause malaria along the border of Thailand and Cambodia, with artemisinin-based treatments the latest set of drugs to fail in this region [Dondorp et al., 2009; Enserink, 2008]. Similarly, viruses—such as the influenza virus—evolve resistance to antiviral drugs [de Jong et al., 2005]. Even vaccines can favor pathogen evolution, including successful evasion of the immune response [Read & Mackinnon, 2007]. Simultaneous with anthropogenic impacts on the evolution of these microorganisms, humans continue to make inroads to wildlife habitats and have greater contact with wildlife through the bushmeat trade, clearing of forest, and expanding human populations along forest edges [Eves et al., 2008]. In response to these threats to biodiversity, a large number of ape sanctuaries have been created to care for injured and orphaned animals [Andre et al., 2008; Beck, 2010; Faust et al., 2011]. The close contact between animals and humans in sanctuaries further increases interspecies contact, especially when the animals interact closely with humans in an effort to provide an appropriate developmental context [Cox & Institute, 2005; Farmer & Courage, 2008; Wobber & Hare, 2011]. The article by Schaumburg et al. [2012] in this issue links these two anthropogenic effects by finding that sanctuary-housed chimpanzees show evidence of colonization by drug-resistant strains of S. aureus found in human populations, including among veterinarians working in the sanctuaries. The results have implications for managing primates, and the authors place their findings in the context of reintroduction efforts. Specifically, the study shows that human pathogens can be introduced to apes destined for release, and thus potentially into wildlife populations. Viewing these organisms as markers for other infectious agents, their presence raises the prospect of substantial pathogen flow from humans to the sanctuary apes, and possibly transmission from apeto-ape, including wild apes. These results are provocative and worthy of further consideration and investigation. In this commentary, we call attention to several questions in the context of these findings, in some cases amplifying points already raised by Schaumburg et al. [2012]. By raising these questions explicitly, we aim to build a clearer picture through synthesis of existing knowledge and identification of new research directions. As a way to frame some of our points, we remind readers of the formula for the basic reproductive number, R0, for directly transmitted microorganisms, such as the bacteria in the Schaumburg et al. [2012] article: