Using bacteria for biocontrol: how Pseudomonas fluorescens defeats the common potato scab

By Steven Harris

Based on a seminar given by Dr Tanya Arseneault written in the style of a Letter to Nature summary paragraph.

Common scab is a potato disease caused by the bacterium Streptomyces scabies (1,2). Streptomyces scabies induces common scab disease by the production of extracellular esterases and the toxin thaxtomin A, which damages the surface of potatoes (Solanum tuberosum) (3,4). Common scab disease is ineffectively controlled currently, with hypotheses suggesting the potential for biocontrol measures to be implemented using Pseudomonas fluorescens (4). Yet the implementation of Pseudomonas fluorescens as a biocontrol has not occurred with the success rate of tuberous crop protection requiring further investigation. Here we show Pseudomonas fluorescens sp. LBUM223 produced the antibiotic phenazine-1-carboxylic acid (PCA) to kill Streptomyces scabies soil pathogens and reduce the virulence of Streptomyces scabies. We found that the production of PCA induced a reduction in thaxtomin A production in Streptomyces scabies, the toxin responsible for common scab disease in potatoes (5,6). Moreover Pseudomonas fluorescens LBUM223 was capable of promoting plant growth regardless of Streptomyces scabies presence. We conclude that decreases in the known virulence factor thaxtomin A enable a reduction in common scab symptoms, increasing potato yield5. Our results express the importance Pseudomonas fluorescens LBUM223 has in future biocontrol of common scab disease, illustrating the possible benefits to agriculture and the field of phytopathology Pseudomonas fluorescens LBUM223 possesses.


1. Han L, Dutilleul P, Prasher S, Beaulieu C, Smith D. Assessment of Common Scab-Inducing Pathogen Effects on Potato Underground Organs Via Computed Tomography Scanning. Phytopathology. 98(10), 1118-1125 (2008)

2. Takeuchi T, Sawada H, Tanaka F, Matsuda I. Phylogenetic Analysis of Streptomyces spp. Causing Potato Scab Based on 16S rRNA Sequences. International Journal of Systematic Bacteriology. 46(2), 476-479 (1996)

3.Kiss, Z., Dobránszki, J., Hudák, I., Birkó, Z., Vargha, G. and Biró, S. (2010). The possible role of factor C in common scab disease development. Acta Biologica Hungarica. 61(3), 322-332 (2010)

4. St-Onge R, Gadkar V, Arseneault T, Goyer C, Filion M. The ability of Pseudomonas sp. LBUM 223 to produce phenazine-1-carboxylic acid affects the growth of Streptomyces scabies, the expression of thaxtomin biosynthesis genes and the biological control potential against common scab of potato. FEMS Microbiology Ecology. 75(1), 173-183 (2010).

5. Arseneault T, Goyer C, Filion M. Pseudomonas fluorescens LBUM223 Increases Potato Yield and Reduces Common Scab Symptoms in the Field. Phytopathology. 105(10), 1311-1317 (2015)

6. Roquigny R, Arseneault T, Gadkar V, Novinscak A, Joly D, Filion M. Complete Genome Sequence of Biocontrol Strain Pseudomonas fluorescens LBUM223. Genome Announcements. 3(3), e00443-15 (2015)

Why do epidemics matter?

By Jennifer Maskell

Based on a seminar given by Professor Jeremy Farrar entitled Why Epidemics Matter.

It is inevitable that emerging diseases and epidemics will continue to impact human populations, more so now than previously because as populations grow, native environments are being increasingly penetrated. Epidemiology is a vital for public health action in order to promote and protect the health of the humans which is founded on scientific study, casual reasoning and “practical common sense” (Bisen, 2013). Epidemiology requires the combination of science and public health practice to tests hypotheses related to the occurrence and prevention of illness and death in order to improve the health of populations throughout the world (Bisen, 2013).

Jeremy Farrar, Professor of Tropical Medicine and Global Health at the University of Oxford and the director of the Wellcome Trust, has devoted much of his life to epidemiology and is known as being an “outstanding clinical scientist” whom is “one of the world’s leading figures in the field of infectious disease” (Wellcome Trust, 2013). Professor Farrar presented the ‘Lowry Lecture’ which focussed on epidemics and their importance. He also addressed various infectious diseases and the problems society and science face with diagnosis, treatment and vaccine development, and discussed why quick response to these diseases is so important.

Professor Farrar first introduced the problems lower income countries face (combination of malaria, tuberculosis and other emerging pathogens, as well as drug resistance) with their poor health and research systems. The aspects of drug resistance was also discussed as being the “largest struggle for the 21st century”, as well as environmental and climate changes affecting the vectors for diseases, and massive urbanisation as being the drive for the way in which epidemics occur. The main focus of the seminar was the comparison of the influenza outbreaks in 1918 and 2009 with the Ebola outbreak in 2014. Professor Farrar claimed the epidemics of influenza were due to poor surveillance of the disease, whereas the Ebola epidemic occurred due to the lack of the response to the disease and to the poor communication. The lack and unnecessarily slow response meant that hospitals in the affected areas were not adequately equipped for treatments for 4-5 months, and within 6 months the rural epidemic became a worldwide epidemic. Even though Ebola had a large impact on health systems and on society and their willingness to trust the government, vaccine trials were accelerated to 6 months (instead of a few years) and luck from these successful trials meant a vaccine could be produced. It is clear to see the importance these accelerated vaccine trials had for the decrease in the spread of the disease. Professor Farrar explained that it is normally the human subject research that limits the speed of a response because the research has become so complicated that scientists are frightened of doing it. A process of human research can take an average of 611 days to be granted and it is predicted that these 611 days can allow for 14 epidemics to arise before the human research process even begins. Professor Farrar concluded that priority for human testing is vital, and it is these changes to such things as human vaccine trials that can help to prepare health systems and to protect populations from such devastating emerging epidemics. To apply these changes for a legally fast response to epidemics like Ebola, he believes the United Nations must reform and the Global Health Leadership has to strengthen. Also, the trust between countries needs to be improved so that treatment can be accelerated. Antibiotic resistance is on the increase, epidemics are inevitable but pandemics are optional.

The main focus of the Lowry Lecture was to highlight the problems in response to epidemics and the need of change to the system by evaluating the influenza and Ebola epidemics. The 1918-1919 Spanish Influenza is a good example used by Farrar that demonstrates the effects of devastating epidemics when response is slow, but also shows the positive outcomes it has for society and the government. The 1918 Spanish Influenza pandemic killed approximately 40 million people within 18 months and is said to have spread around the world approximately 3 times (Kamradt-Scott, 2012). Unlike today, during the late 19th century is was a common thought that the governments had little involvement in ensuring public health. This would have encouraged the lack of response and the rapid spread to the pandemic at this time. Even though influenza epidemics and pandemics occurred frequently, surveillance of cholera and typhoid took over due to their high fatality rates and impacts on international trade. It wasn’t until the 1918 epidemic that societal notions about the disease were changed. The disease became the most devastating event in record human history. What made this pandemic different from previous Influenza outbreaks was the speed at which it travelled across the world, despite the lack of air travel, and its high lethality rate of killing 25% of the entire population (Kamradt- Scott, 2012). As Professor Farrar presented, the disease had a rapid increase of cases and death from the months of September 1918, which peaked with 42 days during November 2014 before rapidly declining a few months later (Holtenius and Gillman, 2014). Similarly to the case Professor Farrar made about the reason for the spread of Ebola, it is believed the reluctance to alert the impact of the disease to other countries aided the spread of the disease. Even though the epidemic caused massive loss to human life, the epidemic lead to a dramatic increase in research of the influenza virus (Potter, 1991). Professor Farrar believes that epidemics are important and this can be viewed in this epidemic as the understandings of pandemic influenza and how best to monitor its effects has improved and altered dramatically overtime as scientific advances were made (which lead to the discovery of a virus being the cause of influenza). More importantly, this pandemic stimulated the creation of vaccines and antiviral medicines to stabilise its symptoms (Kamradt-Scott, 2012). The increasing understanding of the Spanish Influenza also helped with the fast response to the H1N1 strain of influenza that caused a pandemic in 2009. Like Professor Farrar explained, the H1N1 strain followed the same infectivity rates as the 1918 influenza pandemic, and although less severe than was originally feared, the virus was detected in multiple countries within weeks. Due to its similarity to the H1N1 strain, response was fast and contingency plans were enforced, emergency committees were assembled and the process of acquiring relevant antivirals and vaccines were initiated (Kamradt-Scott, 2012). This response was only possible due to a comprehensive medical infrastructure and appropriate funding, as well as international and national bodies who kept the public fully informed. They also made a potential outbreak in developing countries a matter of grave concern (Jivraj and Butler, 2013). Although authorities overreacted to this pandemic, like Professor Farrar explained in his seminar, it is good to overreact occasionally to epidemics such as these so that we are able to contain certain diseases that are of importance. For example, this was not the case for the Ebola outbreak in 2014 – as stated by Professor Farrar – that had devastating impacts on health systems, society and the willingness of communities to trust the government. Professor Farrar claimed that the reason for the failure to act on the Ebola epidemic was due to it occurring in a challenging part of the world that had complex government systems (just come out of a civil war). Although this is true, it took the World Health Organisation 3 months to declare the Ebola virus disease as an epidemic (WHO Ebola Response Team, 2014) which suggests that initial recognition and communication about the disease cases, along with the global response were highly inadequate and posed as the initial problems to the spread of the disease. This delay caused postponements in the deployments of experts and medical materials and treatment centres which finally arrived when the virus was already out of control (World Health Organisation, 2014). There were also no known vaccines or efficient vaccines. It is surpsinging that authorities did not respond more quickly to the outbreaks as it spread to communities so quickly and mortality rates were so high. The Ebola epidemic of 2014 did however have a positive outcome (which reflects Professor Farrar’s motives of improving the authority and legality for faster responses to emerging epidemics), in that it lead to accelerated vaccine trials. A process that normally takes a few years, were accelerated to 6 months without compromising the policies for vaccine safety and efficiency (World Health Organisation, 2015). The Ebola vaccine trials took the “risk-based approach” that focuses on a centralised monitoring method (Roca, et al., 2015). It was this approach which (although slightly luck-based) lead to the fast admission of vaccines that has helped to reduce the spread of the disease across multiple affected countries. Due to Ebola’s high mortality rates and the speed at which it spreads, accelerated vaccine trials such as these were granted. This case just proves how vital a fast response is. If authorities had declared the outbreak sooner, this accelerated vaccine trial may either not have been needed, or it could have been initiated much sooner at the start of its discovery which could have later saved thousands of lives.

This topic is something Professor Farrar expressed in the Lowry Lecture – in that changes to response and changes to clinical policy can allow for such dramatic responses. He explains the standards need reforming, and as seen from such a devastating effects of Ebola it is evident to see why this is so important. Without such epidemics and without the problems of response they have raised, the health sector may still react this way to emerging pathogens in years to come. Professor Farrar’s motives are right; transformations are needed in order to successfully and rapidly respond to emerging public health emergencies. Although rapid response and better communication is needed, it is also of importance that health centres are always prepared to care for patients with lethal infectious diseases in order to help prevent the spread of emerging epidemics. Developments in appropriate research protocols approved for clinical research to begin immediately once a future epidemic threatens is going to be vital for the future, especially as antibiotic resistance is becoming a threat to the human population. It should be noted that, as Professor Farrar believes, “experience confirms that the time to act is now” (Dunning, et al, 2014).


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