Abstract
As human populations grow and transform landscapes, contact with wildlife concomitantly increases. Disease emergence has been an important consequence of these contacts, with many of emerging infectious diseases in humans arising from wildlife reservoirs. Drug resistance is a very important dimension of disease emergence and tracing the source is a veritable containment strategy. Escherichia coli and Proteus spp. have important roles in the increasing cases and dissemination of antibiotic resistance, potentially acquiring resistance determinants and acting as reservoirs for resistance genes. This study was conducted to determine the similarity or otherwise of the drug resistance pattern of Escherichia coli and Proteus spp. isolated from humans and those from wild animals (a source with only minimal, hypothetical or no antibiotic exposure). The human samples were obtained from two human groups: persons not on antibiotics and humans on antibiotics. Animal samples were taken from rats (Rattus spp.), grasscutters (Thryonomys swinderianus), squirrels (Xerus erythropus) antelopes (Tragelephus scriptus), rabbits (Oryctolagus cuniculus), and farm lizards (Agama spp.). Organisms were isolated and identified based on basic microbiological methods and subjected to antibiotic disc diffusion tests and electrophoretic plasmid analysis. Results show that E. coli strains isolated from persons on antibiotics were resistant to ampicillin (46.62%), augmentin (39.72%), clarithomycin (5.16%); while resistance to antibiotics by E. coli isolated from those that are not on antibiotics were ampicillin (27.27%), augmentin (20.00%), cetriaxone (18.18%) and nitrofurantoin (14.55%). Also, E. coli strains isolated from wild life were resistant to ampicillin (85.71%) and clarithomycin (14.29%). Proteus spp. isolated from human sources were susceptible to all test antibiotics except ampicillin; while those from wildlife were resistant to ampicillin (54.17%), chlorampenicol (16.67%), nitrofurantoin (8.33%), clarithomycin (8.33%), ofloxacin (4.17%), augmentin (4.17%) and pefloxacin (4.17%). The correlation matrices determined at p (≤ 0.05), revealed high resistance correlation among the different genera of bacteria isolated from one source to those from the other sources. Resistance plasmid analysis revealed the presence of 23 kb plasmid DNA in organisms obtained from the different sources. This suggests the possibility of bidirectional resistant gene transmission at the human–wildlife interface, indicating congruence between the drug resistance pattern of E. coli and Proteus spp. isolated from humans and wild animals. This calls for a holistic and forward-looking approach that will take the complex interconnections among species into full account, recognizing the important link between humans, animals and the environment in a bid to contain antibiotic resistance. Key words: Drug resistance, humans, wild animals, Escherichia coli, Proteus spp., resistance plasmids.
Highlights
As human populations grow and transform landscapes, contact with wildlife concomitantly increases
Disease emergence has been an important consequence of these contacts, with many of emerging infectious diseases in humans arising from wildlife reservoirs
Proteus spp. isolated from human sources were susceptible to all test antibiotics except ampicillin; while those from wildlife were resistant to ampicillin (54.17%), chlorampenicol (16.67%), nitrofurantoin (8.33%), clarithomycin (8.33%), ofloxacin (4.17%), augmentin (4.17%) and pefloxacin (4.17%)
Summary
As human populations grow and transform landscapes, contact with wildlife concomitantly increases. Human modification of the environment is seen as the primary driver of the emergence of zoonotic diseases, through providing the opportunity for direct and indirect contact between humans and (sympatric) wildlife and increasing pathogen exposure and transmission potential (Mayer, 2000; Deem and Karesh, 2001; Pesapane et al, 2013). Disease emergence has been an important consequence of this escalation in interaction, with the majority of emerging infectious diseases in humans arising from wildlife reservoirs (Jones and Petel, 2008). These changes can induce immediate as well as long-term effects on pathogen transmission dynamics, modifying genetic and biological characteristics, biophysical elements, ecological dynamics, and socioeconomic, as well as host(s)–pathogen interactions (Smolinski and Hamburg, 2003). Some of the most devastating and persistent human pathogens can be traced to zoonotic origins
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