“This report of EFSA and the European Centre for Disease Prevention and Control presents the results of the zoonoses monitoring activities carried out in 2015 in 32 European countries (28 Member States (MS) and four non-MS). Campylobacteriosis was the most commonly reported zoonosis and the increasing European Union (EU) trend for confirmed human cases since 2008 continued. In food, the occurrence of Campylobacter remained high in broiler meat. The decreasing EU trend for confirmed human salmonellosis cases since 2008 continued, but the proportion of human Salmonella Enteritidis cases increased. Most MS met their Salmonella reduction targets for poultry. More S. Enteritidis isolates were reported and S. Infantis was confirmed as the most frequent serovar isolated from domestic fowl. In foodstuffs, the EU level Salmonella non-compliance for minced meat and meat preparations from poultry was low. Despite the significant increasing trend since 2008, the number of human listeriosis cases stabilised in 2015. In ready-to-eat foods, Listeria monocytogenes seldom exceeded the EU food safety limit. The decreasing EU trend for confirmed yersiniosis cases since 2008 continued. Positive findings for Yersinia were mainly reported in pig meat and products thereof. The number of confirmed shiga toxin-producing Escherichia coli (STEC) infections in humans was similar to 2014. In food, STEC was most frequently reported in meat from ruminants. A total of 4,362 food-borne outbreaks, including waterborne outbreaks, were reported. Bacteria were the most commonly detected causative agents, followed by bacterial toxins, viruses, other causative agents and parasites. The causative agent remained unknown in 33.5% of all outbreaks. As in previous years, Salmonella in eggs continued to represent the highest risk agent/food combination. The report further summarises trends and sources for tuberculosis due to Mycobacterium bovis, Brucella, Trichinella, Echinococcus, Toxoplasma, rabies, Coxiella burnetii (Q fever), West Nile virus and tularaemia.”
There are fears that Africa’s next major modern disease crisis will emerge from its cities. Like Ebola, it may well originate from animals. Understanding where it would come from and how this could happen is critical to monitoring and control.
Growth and migration are driving huge increases in the number of people living in Africa’s urban zones. More than half of Africa’s people are expected to live in cities by 2030, up from about a third in 2007.
The impact of this high rate of urbanisation on issues like planning, economics, food production and human welfare has received considerable attention. But there hasn’t been a substantive effort to address the effects on the transmission of the organisms – pathogens – that cause disease. This is despite several influential reports linking urbanisation to the risk of emerging infectious diseases.
Africa’s cities are melting pots of activity and interaction. Formal and informal trading take place side by side. The wealthy live alongside the poor, livestock alongside people and waste is poorly disposed of near food production areas.
This degree of mixing and contact creates an opportune ecological setting for pathogen transmission for a variety of bugs. Already approximately 60% of human pathogens are zoonotic. This means that three out of five human diseases are transmitted from animals. Scientists predict that this is set to increase and that about 80% of new pathogens will have zoonotic origins.
Emerging infectious diseases are a major concern to the global public health community, both in terms of disease burden and economic burden. Understanding the processes that lead to their emergence is therefore a scientific research priority.
Over the last five years I have been working with a group of researchers to understand what leads to the introduction of pathogens in urban environments and how those then emerge in the human population.
Tracking the next disease
Investigating the pathogens we already know about can help us understand the mechanisms and processes that underlie the emergence of new pathogens.
The questions that need to be addressed are:
- what is it about urban environments that might predispose to an emergence event, and
- what is the relevance of livestock as reservoirs of potentially emerging pathogens in these environments?
What’s been lacking from a public health perspective are studies linking wider ecological systems – such as intensive farming systems – to disease emergence and human social organisation. Also missing are studies that investigate the diversity of micro-organisms at a genetic level in these settings – a field called microbial genetics. This kind of research is not often undertaken on a meaningful scale.
The work that we’ve been doing in Kenya’s capital Nairobi aims to go some way towards plugging this gap.
Urban zoo project
Our Urban Zoo project, funded by the UK Medical Research Council and other UK research councils, has focused on livestock as a major source of emerging zoonotic diseases. This is a critical interface as 40% of known livestock pathogens (200 species) can infect humans.
We’ve been taking a landscape genetics approach to understand how urban populations connect to livestock. This means we study the pathogens and their hosts from an ecological perspective. It’s a fascinating way to do science on a big scale. We investigate humans in different socio-economic groups, the peri-domestic wildlife that live around them, the livestock they keep and the livestock that feed them.
Our method of choice is to explore the diversity of the bacterium Escherichia coli as an exemplar. E. coli is an excellent microbe to study for this purpose. It is zoonotic, exists in many hosts and in the environment, and can be found in food products of animal origin.
We have also been:
- Mapping animal source food systems – in both the formal and informal sectors – that bring food to city residents
- Trying to understand human relationships with livestock in the city itself. This is a social science and economic approach that explores why people keep animals and how they contribute to their livelihoods
- Factoring in public health, environmental, social and ecological characterisation of the city. For example, we’ve mapped low income neighbourhoods using cameras on hot air balloons to see how food sellers are distributed in a bacteria-rich environment
As a global scientific community, and as providers of evidence to those who make policy, we need to be able to explain the mechanisms behind issues such as this. Only when we have achieved this will the risk of disease emergence in these settings be relevant to those responsible for mitigating its occurrence. The risks must be balanced against the benefits of allowing city environments to provide a livelihood for their residents.
A recent (16 August 2016) publication by Arnold et al. tries to dymistify “the possible role of wildlife in the dissemination of AMR, specifically how wildlife might acquire and transport AMR and the potential for them to transmit AMR to humans and livestock.”
The authors note that “little is known about the flow and fate of AMR in the natural environment”, I believe the ongoing research on wildlife in Nairobi may address some the research gaps presented in the paper.
Read the paper here: http://dx.doi.org/10.1098/rsbl.2016.0137
A simple question am left wondering are wildlife the “threat” or are they the “victims of a threat of our own making”?
Have a nice read. Drop your comments below.
Staphylococcus aureus is an important bacteria because of its ability to cause a wide range of diseases and adapt to diverse environments. The bacteria causes infection to both humans and animals by colonizing their skin, skin glands and mucous membranes, resulting to septicemia, meningitis, and arthritis in man and mastitis in the bovine, as well as poultry limb infections . Methicillin-resistant Staphylococcus aureus (MRSA) is a type of staphyloccocal bacteria that is resistant to beta-lactams. It is a common cause of healthcare-associated infections in both developed and developing countries, though limited information is available from the latter  .
MRSA Resistance mechanisms
The resistance of S. aureus against methicillin is caused by expression of Penicillin binding protein 2A (PBP2A) encoded by the mecA gene . PBP2A has low affinity for beta-lactam antibiotics such as amoxicillin, methicillin and oxacillin, rendering these antibiotics ineffective in treating infections caused by Staphylococcus aureus. Lately, a new methicillin resistance mechanism gene, mecC has been reported in isolates from humans and animals . This therefore means that MRSA is not only associated with prior exposure to a health care facility but also raises concerns for infections originating from the community and veterinary species, and there is a possibility of a cross-infection with animals being potential sources of MRSA infection to humans .
MRSA the Kenyan perspective
In 1997, documented rates of MRSA in Kenya were 28 percent of all S. aureus tested in city hospitals. A separate hospital-based study during the same year found the prevalence of MRSA to be 40 percent of all S. aureus infections. In 2006, MRSA was found in 33 percent of S. aureus isolates at another hospital based study . Resistance, therefore, may indicate illegal use of drugs by the public. A survey of farmers in Kenya found that the majority conflated treatment with prevention, effectively replacing hygiene and feeding practices as standard disease prevention with disease treatment . Patterns of resistant Staphylococcus aureus in cattle imply a significant difference in resistance profiles of large and small scale farms, with smaller producers using nearly twice the amount of antibiotics per animal compared with larger producers . The prevalence of multidrug resistance, at 34 percent on small farms, was likewise almost double the rate found at large farms .
There is evidence that MRSA infection increases the risk of mortality, morbidity, medical care costs and loss of productivity. The increased medical care costs accrued directly as expenses caused by extension of hospital stay, additional diagnostic or therapeutic procedures, and additional antibiotic use while loss of productivity is due to absence from work during hospitalization. At the same time, published data concerning the antibiotic susceptibility patterns of MRSA in sub-Saharan Africa are extremely limited, and few studies on it have been conducted in Kenya  . Many studies on MRSA in Kenya are mainly cross-sectional with a focus to determine the prevalence, identifying the antibiotic resistance but they have not focused on the zoonotic significance of MRSA. There is need to understand on how the resistance to MRSA is changing over time so as to be able to clearly visualize the mechanism and transfer of resistance genes in the population .
Zoonotic directionality of resistance
It is therefore important not only to determine the antibiotic resistance, but also determine what and who is causing this resistance in humans and animals belonging to the same household and also determine the temporal and spatial change of this resistance over time. This is because, by understanding the dynamics and the epidemiology of MRSA infection over time it will be possible to develop more informed prevention and control strategies, develop more sound policies including education on the rational use of antibiotics to the public. At the same time it is important to fill the knowledge gap  (especially from a developing country setting) in the zoonotic directionality of MRSA.
Waldvogel, F.A., Staphylococcus aureus, in Principles and practices of infectious disease, G.L. Mandell, D. R.G., and B. J.E., Editors. 2000, Pennsylvania, USA.: Churchill Livingstone, Philadelphia, . p. 1754-1777.
Global Antibiotic Resistance Partnership-Kenya Working Group, Situation Analysis and Recommendations: Antibiotic Use and Resistance in Kenya, S. Kariuki, Editor. 2011, Center for Disease Dynamics, Economics & Policy: Washington, DC and New Delhi.
WHO, Antimicrobial resistance global report on surveillance. 2014. p. 1-256.
Wielders, C.L.C., et al., mecA Gene Is Widely Disseminated in Staphylococcus aureus Population. J. Clin. Microbiol., 2002. 40(11): p. 3970-3975.
Paterson, G.K., et al., The newly described mecA homologue, mecALGA251, is present in methicillin-resistant Staphylococcus aureus isolates from a diverse range of host species. J. Antimicrob. Chemother., 2012. 67(12): p. 2809-2813.
Ferreira, J.P., et al., Transmission of MRSA between Companion Animals and Infected Human Patients Presenting to Outpatient Medical Care Facilities. PLoS ONE, 2011. 6(11): p. e26978.
Shitandi, A. and A. Sternesjö, Prevalence of Multidrug Resistant Staphylococcus aureus in Milk from Large and Small Scale Producers in Kenya. Journal of Dairy Science, 2004. 87: p. 4145-4149.
The finding points to ways that ‘superbugs’ might spread
Antibiotic-resistance is a major concern with far-reaching effects. Bacteria that can shrug off the drugs meant to kill them pop up all over the world — in ancient feces, in isolated cultures of people who have never taken antibiotics, and even in the Hudson River. Now researchers have found such microbes in African wildlife, reports Jennifer Balmer for Science.
Two researchers, Sarah Elizabeth Jobbins and Kathleen Ann Alexander, tested Escherichia coli strains for resistance to 10 commonly used antibiotics, they report in the Journal of Wildlife Diseases. More than 40 percent of the animals tested — including hyena, crocodile, leopard, bushbuck, giraffe and baboon — carried E. coli resistant to one antibiotic and more than 13 percent were resistant to three or more. More than 94 percent of humans tested carried strains resistant to one antibiotic and nearly 69 percent were resistant to three or more antibiotics. The implication is that the relationship isn’t coincidental.
The resistance may have traveled through water contaminated with human fecal matter via sewage and stormwater runoff, the researchers write. The water-dwelling animals had higher levels of antibiotic resistance than those that lived on land.
“Alarmingly, we demonstrated widespread resistance in wildlife to several first-line antimicrobials used in human medicine—ampicillin, doxycycline, streptomycin, tetracycline, and trimethoprim– sulfamethoxazole (commonly known as cotrimoxazole),” the researchers write. Doxycycline, they note, is often used by visitors to Africa to protect against malaria. Cotrimoxazole is given to HIV patients to protect against infection. Widespread resistance to those drugs may someday render them useless as medicine.
This article originally appeared on news section of the smithsonianmag website.
Washington, DC – August 20, 2015 – Swedish exchange students who studied in India and in central Africa returned from their sojourns with an increased diversity of antibiotic resistance genes in their gut microbiomes. The research is published 10 August in Antimicrobial Agents and Chemotherapy, a journal of the American Society for Microbiology.
In the study, the investigators found a 2.6-fold increase in genes encoding resistance to sulfonamide, a 7.7-fold increase in trimethoprim resistance genes, and a 2.6-fold increase in resistance to beta-lactams, all of this without any exposure to antibiotics among the 35 exchange students. These resistance genes were not particularly abundant in the students prior to their travels, but the increases are nonetheless quite significant.
The germ of the research was concern about the burgeoning increase in antibiotic resistance. “I am a physician specializing in infectious diseases, and I have seen antibiotics that I could safely rely on ten years ago being unable to cure my patients,” said principal investigator Anders Johansson, MD, PhD, Chief, Infection Control, Umeå University and the County Council of Våsterbotten, Sweden.
However, Johansson also questioned the conventional wisdom that overuse of antibiotics was entirely responsible for the surge in resistance, despite the fact that overuse is a huge problem. “Currently, I head an infection control department, and from this position it is very evident that resistance is no longer generated primarily in the hospital,” he explained. Instead, patients bring bacteria carrying resistance genes into the hospital as part of their own microbial communities, he said. “We hypothesized that the gut microbiome of humans serves as a vehicle for moving many different resistance genes very large distances, even in the absence of antibiotic treatment.”
And in fact, the increases the investigators observed in abundance and diversity of resistance genes occurred despite the fact that none of the students took antibiotics either before or during travel. The increase seen in resistance genes could have resulted from ingesting food containing resistant bacteria, or from contaminated water, the investigators write. Providing further support for the hypothesis that resistance genes increased during travel, genes for extended spectrum beta-lactamase, which dismembers penicillin and related antibiotics, was present in just one of the 35 students prior to travel, but in 12 students after they returned to Sweden.
Collecting samples of resistance genes was simple. “We asked students going abroad on exchange programs to provide a sample of their feces before and after traveling,” said Johansson. But the study was different from previous studies of this issue in using metagenomics sequencing, a modern method. That enabled the investigators to sample the entire microbiome of each student, and to sequence every resistance gene therein, rather than focusing on resistance genes in those few bacterial species that grow well on culture plates.
“Our results spotlight that to reduce antibiotic resistance we need to minimize dispersal rates from the healthcare system, and importantly, at the societal level,” said Johansson. Suppressing further spread after travelers return to their home countries is crucial, and depends, he added, upon having well-informed citizens and a well-functioning public health system.
This article originally appeared on the EurekAlert website.