The 'Battling Bacteria' science outreach session and all associated resources have been designed as part of a Cell EXPLORERS project by 4th year NUI Galway Microbiology students Kenneth Farrell, Grainne Kennedy, Conor Hession and Sinead Woods in Oct-Nov 2015. Each blog post below is the individual work of the author as named.
The session was piloted with Mr Barry McGuire and his 6th class students at Galway Educate Together NS.
The 'Battling Bacteria' webpage has been designed and built by Sinead Woods.
A fun, interactive educational outreach resource about Antibiotics and Antibiotic Resistance.
Want to find out more?
Read the blogs and try the resources yourself
Antibiotics have saved the lives of a countless number of people since Alexander Fleming’s discovery of penicillin in 1928. In recent times antibiotics have been becoming less and less effective at treating bacterial infections. Why is this so? It is because of Antibiotic Resistance.
Bacteria won’t go down without a fight!
Is antibiotic resistance when my body builds up a tolerance to antibiotics? No! This is not the case in fact it is one of the most common misconceptions around the topic of antibiotic resistance. Antibiotic resistance is when bacteria become resistant to the effects of an antibiotic.
Fig.1: A cartoon depicting the fight between antibiotics and resistant bacteria (Wales.nhs.uk, 2015)
But how does bacteria becoming resistant to antibiotic affect me?
As Explained in the “Microbiology and microbial interactions” blog different microorganisms are responsible for causing different illness bacteria, fungi and viruses. In the Antibiotics blog it is explained that antibiotics treat illness caused by bacteria. They do so by destroying the bacteria that are causing us to feel sick. Well if the bacteria that are causing us to feel sick can no longer be destroyed by a certain antibiotic then the illness the bacteria are causing will not go away when treated with this antibiotic. Therefore you will still feel sick even after taking this antibiotic.
How do these bacteria become resistant?
In the previous blog about antibiotics it is explained how antibiotics target specific structures in order to destroy bacteria. Changes in these structures allow for bacteria to become resistant to the effects of the antibiotic. Bacteria acquire these changes usually through mutations in their genetic structure. Mutations in there genetic structure can lead to changes in their physical structure. It is the changes in the bacteria’s physical structure that allow them to become resistant to antibiotics.
There are 4 main ways that bacteria change to become resistant;
Some bacteria change the structure of the proteins that the antibiotics attach to. A good example of this is bacteria that become resistant in this way are the bacteria that become resistant to penicillin. These bacteria change the structure of the protein that penicillin attaches to. If penicillin can no longer attach to this protein then the cell wall of the bacteria will not be broken down. The bacteria that causes strep throat (Streptococcus pyogenes) can become resistant to penicillin in this way. (Tenover, 2006)
Some bacteria change so that they produce more of a special type of protein. These proteins are capable of inactivating the antibiotic that is targeting them. Staphylococcus aureus, a bacteria which causes skin infections can become come resistant to the antibiotic erythromycin this way (Eady et al., 1993; Tenover, 2006).
Some bacteria can change the shape of their outer membranes so that the antibiotic can no longer enter the bacteria. An example of this would be the E. coli bacteria that cause illnesses such as urinary tract infections. These bacteria can change their outer membranes to become resistant to antibiotics such as tetracycline (Pourahmad Jaktaji and Heidari, 2013;Tenover, 2006).
Some bacteria acquire a change that allows them to create more structures that expel the antibiotic from the cell stopping the antibiotic from eliminating them. An example of bacteria that can acquire this change is Staphylococcus aureus that are resistant to fluoroquinolone antibiotics. (Kaatz et al., 1993) (Tenover, 2006)
A few resistant bacteria can lead to an army of resistant bacteria!
Imagine if initially just a few of your bacteria were resistant to an antibiotic. When you take the antibiotic to cure your illness the antibiotic will be effective at eliminating the illness. This is because there were only a few bacteria out of all the bacteria that were causing the illness that were resistant. These few bacteria will still survive in your body even though the symptoms of the illness may be gone. These few resistant bacteria can multiply and multiply until they cause the illness again. When you take the same antibiotic that you did the first time, the antibiotic will no longer be effective against the illness because it is now being caused by a population of resistant bacteria.
Bacteria are also capable of passing on their resistance to other bacteria. Resistant bacteria can pass their resistance onto other bacteria to create an even larger population of resistant bacteria. This idea is represented in Fig.2 (Cdc.gov, 2015)
Fig. 2: How populations of resistant bacteria are formed. (Cdc.gov, 2015)
How could I acquire these harmful antibiotic resistant bacteria?
Not finishing the course prescribed to you by the doctor can cause some of the harmful bacteria to still survive in your body. Some of these bacteria could acquire a mutation that caused them to be resistant to an antibiotic. As mentioned earlier in this blog these bacteria could form a population of harmful resistant bacteria.
Taking antibiotics when they are not need also could cause harmless bacteria to acquire a mutation. As mentioned already in this blog bacteria are capable of passing on their resistance. These harmless bacteria could pass on their resistance to harmful bacteria.
From other people
Harmful antibiotic resistant bacteria can spread amongst people the exact same way non-resistant bacteria spread amongst people. Imagine a patient was prescribed antibiotics to treat their illness. This patients bacteria could become resistant to this antibiotic. If this patient visited the hospital then there resistant bacteria could spread to other patients in the hospital through bad hygiene and unclean facilities. After this the resistant bacteria that have been spread to the patients in the hospital could be spread to the general public when these patients interact outside the hospital.
Antibiotic resistant bacteria can even be spread from animals to humans. Animals can acquire resistant bacteria when given antibiotics. The resistant bacteria can be spread from animals to the general public through direct contact with the animals, through food (eating these animals) or through the environment
Can some of these resistant bacteria become resistant to more than one antibiotic?
Yes! Some bacteria can become resistant to more than one antibiotic. These bacteria are known as “Super bugs”. An example of a superbug that is causing problems in the world today is methicillin resistant Staphylococcus aureus. Bacteria becoming resistant to multiple types of antibiotics is something that should be worried about. If these bacteria acquire even more resistance it could lead to bacteria in which no antibiotic is capable of destroying. Measures need to be taken to prevent the spread of these super resistant bacteria. The Measures are dealt with in the “Racing resistance” blog as well as more information on “Super bugs (Cdc.gov, 2015).
Spread the word before the resistant bacteria spread
It is important that more people are informed about antibiotic resistance so that they can understand the dangers of it. A resource can be found on this site that is designed to teach primary school students about antibiotics and antibiotic resistance in a fun way
Cdc.gov, (2015). General Information | Healthcare Settings | MRSA | CDC. [online] Available at: [Accessed 17 Nov. 2015].
Cdc.gov, (2015). About Antimicrobial Resistance| Antibiotic/Antimicrobial Resistance | CDC. [online] Available at: [Accessed 17 Nov. 2015].
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Levy, S. (1998). The Challenge of Antibiotic Resistance. Sci Am, 278(3), pp.46-53.
Pourahmad Jaktaji, R. and Heidari, F. (2013). Study the Expression of ompf Gene in Esherichia coli Mutants. Indian J Pharm Sci, 75(5), pp.540–544
Tenover, F. (2006). Mechanisms of antimicrobial resistance in bacteria. American Journal of Infection Control, 34(5), pp.S3-S10.
Wales.nhs.uk, (2015). Abertawe Bro Morgannwg University Health Board | Antibiotic Resistance. [online] Available at: [Accessed 3 Dec. 2015].
Who.int, (2015). WHO | World Health Organization. [online] Available at: [Accessed 2 Dec. 2015].
Antibiotic Resistance, when bacteria fight back!
by Conor Hession
What are antibiotics?
Antibiotics are medicines which when taken carefully can eliminate a bacterial infection. Natural products produced by microbes are in fact the source of most of the antibiotics that exist in our world today (Peláez, 2006).
When should antibiotics be taken?
Antibiotics should only ever be taken if directed to do so by your doctor.
A doctor should only prescribe youan antibiotic if a bacterial infection is
present. If thedoctor believes the infection present is caused by a virus
or another source, an antibiotic should not beprescribed. Use of antibiotics
when a bacterial infectionis not present is a threat to our health. Whilst the
knowledge behind the use of antibiotics exists there still remains the issue
of common misconceptions from the public associated with the use of
antibiotics (See Fig 1.)
How do antibiotics work?
Serval different types of antibiotics have come to market since the
discovery of antibiotics in the early 20th Century (Zaffiri et al., 2012).
Antibiotics have successfully treated bacterial infections by targeting
specific processes that bacteria conduct in order to survive (Kohanski et
al., 2007), (See Table 1). The class of antibiotics determines the
drug-target interaction and the resulting outcome of the bacterial cell
(Kohanski et al., 2007). The main targets of antibiotics are listed in Table 1
with a brief explanation of the cellular purpose of each target in Table 2.
Peptidoglycan biosynthesis will be discussed in more detail below.
Although not listed in Table 1 each class of antibiotic subjects one of two
possible outcomes on a bacterial cell post interaction. These outcomes
depend on whether the antibiotic is bacteriostatic; in which case further
growth of the cell will be inhibited, or bactericidal; which will result in
immediate cell death (Kohanski et al., 2007).
Beta Lactams & Peptidoglycan Biosynthesis
Peptidoglycan is the main component of the bacterial cell wall, a component essential to cell survival due to its central role in controlling the strength and rigidity of the cell (Scheffers & Pinho, 2005). It’s made of many layers of long chains of polysaccharides (sugars) cross-linked via short chains of amino acids. (Morin & Gorman, 2014)(See Figure 2). Cross-linking of the amino acid chains is achieved using a penicillin-binding protein (See Figure 3)
Beta lactams are the eldest and most widely used antibiotic in the world (Dougherty and Pucci, 2012). Bactericidal in nature they destroy bacterial cells by inhibiting peptidoglycan synthesis. Penicillin achieves this by binding to the PBPs (See Figure 4), and prevents them from forming the bond between adjacent chains of amino acids, thus preventing crosslinking of
peptidoglycan layers (Kohanski et al, 2010)(SeeFigure 5). Disruption in cell wall formation interferes with
osmotic regulation thus causing the cell to burst and lyse.
The history of antibiotics & their impact of antibiotics on society
Antibiotics were first discovered in the early 1900’s and have since had a massive impact on society over the last century, curing many illnesses and saving thousands of lives (Kohanski, 2010). Penicillin was the first antibiotic to be discovered. It was accidentally discovered in 1928 in a laboratory belonging to Alexander Fleming, a bacteriologist, searching for cures for bacterial infections. He noticed the growth of mould on his bacteria plate, a common contamination issue to most microbiologists, but more so the region of clearance around the mould where the colonies of bacteria no longer existed. Isolating the mould he made an antibacterial substance however it wasn’t until ten years later in 1938 when Ernst Chain and Howard Florey assembled a team at oxford to understand the chemotherapeutic action behind Penicillin (Ban, 2006). The discovery of Penicillin led to the developments of many other antibiotics, a development considered to be one of the biggest achievements of modern science. Since the initial discovery serval different types of antibiotics have come to market (Zaffiri et al., 2012).
The introduction of antibiotics in the early 1900’s tremendously impacted on society banishing the threats associated with diseases such as tuberculosis, pneumonia, diphtheria and diarrhoea which were the main causes of morbidity and mortality at the time. The discovery of penicillin caused a decline of 90% in morbidity and mortality rates in syphilis between 1945 and 1975 and streptomycin combined with three other antibiotics resulted in 90-95% cured Tuberculosis patients (Zaffiri et al., 2012).
Throughout the 20th Century pharmaceutical companies profited hugely on this this discovery however the need for new antibiotics was declared a low priority research area in the late 1960’s due to a rise in mortality rates and a decline in industry funding (Overbye & Barrett, 2005). Coinciding with the reduction in production of new antibiotics a dangerous trend in the increase of antibiotic resistance was recognised (Wallmann, 2014). The key driver of this emergence was established as the human misuse and abuse of antibiotics (Davies & Davies, 2010). With the efficiency of antibiotic activity failing incidence of disease and death are on the increase once again. According to the US Centers for Disease Control and Prevention, current estimates state that each year approximately 2 million people are affected by antibiotic-resistantance whilst at least 23 000 deaths occur as a result of resistant bacterial infections (Gualano et al., 2014).
It is evident that this worldwide problem does not have a simple solution however there is reason to believe that various implementations such as efforts are being made to inform the public on appropriate methods when using antibiotics (Lecky et al., 2014) and resuming the search for new antibiotics may slow down the rate at which antibiotic resistance is emerging (Davies & Davies, 2010).
Ban, T. A. (2006). The role of serendipity in drug discovery. Dialogues in clinical neuroscience, 8(3), 335.
Cooper, G. and Hausman, R. (2007). The cell. Washington, D.C.: ASM Press.
Davies, J. and Davies, D. (2010). Origins and Evolution of Antibiotic Resistance. Microbiology and Molecular Biology Reviews, 74(3), pp.417-433.
Dougherty, T. and Pucci, M. (2012). Antibiotic discovery and development. New York: Springer, pp.79-117.
Gualano, M., Gili, R., Scaioli, G., Bert, F. and Siliquini, R. (2014). General population's knowledge and attitudes about antibiotics: a systematic review and meta-analysis. Pharmacoepidemiology and Drug Safety, 24(1), pp.2-10.
Kohanski, M., Dwyer, D. and Collins, J. (2010). How antibiotics kill bacteria: from targets to networks. Nature Reviews Microbiology, 8(6), pp.423-435.
Kohanski, M., Dwyer, D., Hayete, B., Lawrence, C. and Collins, J. (2007). A Common Mechanism of Cellular Death Induced by Bactericidal Antibiotics. Cell, 130(5), pp.797-810.
Lecky, D., Hawking, M., Verlander, N. and McNulty, C. (2014). Using Interactive Family Science Shows to Improve Public Knowledge on Antibiotic Resistance: Does It Work?. PLoS ONE, 9(8), p.e104556.
Morin, R. B., & Gorman, M. (Eds.). (2014). The Biology of B-Lactam Antibiotics. Elsevier. (Vol. 3). p. 212
Overbye, K. and Barrett, J. (2005). Antibiotics: Where did we go wrong?. Drug Discovery Today, 10(1), pp.45-52.
Peláez, F. (2006). The historical delivery of antibiotics from microbial natural products—Can history repeat?. Biochemical Pharmacology, 71(7), pp.981-990.
Scheffers, D. J., & Pinho, M. G. (2005). Bacterial cell wall synthesis: new insights from localization studies. Microbiology and Molecular Biology Reviews. 69 (4). p.585-607.
Vanden Eng, J., Marcus, R., Hadler, J., Imhoff, B., Vugia, D., Cieslak, P., Zell, E., Deneen, V., McCombs, K., Zansky, S., Hawkins, M. and Besser, R. (2003). Consumer Attitudes and Use of Antibiotics. Emerg. Infect. Dis., 9(9), pp.1128-1135.
Wallmann, J. (2014). Antimicrobial resistance: challenges ahead. Veterinary Record, 175(13), pp.323-324.
Witthoff, S., Muhlroth, A., Marienhagen, J. and Bott, M. (2013). C1 Metabolism in Corynebacterium glutamicum: an Endogenous Pathway for Oxidation of Methanol to Carbon Dioxide. Applied and Environmental Microbiology, 79(22), pp.6974-6983.
Zaffiri, L., Gardner, J. and Toledo-Pereyra, L. (2012). History of Antibiotics. From Salvarsan to Cephalosporins. Journal of Investigative Surgery, 25(2), pp.67-77.
Konings, W. N., Albers, S. V., Koning, S., & Driessen, A. J. (2002). The cell membrane plays a crucial role in survival of bacteria and archaea in extreme environments. Antonie Van Leeuwenhoek, 81(1-4), 61-72.
by Grainne Kennedy
Microbiology & Microbial Interactions
by Kenneth Farrell
What is microbiology and why is it important?
Microbiology is the scientific study of microorganisms (or “microbes”), microscopic living things. The three most common types of microbe are bacteria, fungi and viruses. Viruses, although widely regarded as microorganisms, are generally thought of as non-living. Microbes can be found everywhere on the planet from the most extreme environments, such as hydrothermal vents deep beneath the oceans, to common household surfaces and even inside our bodies. It is estimated that there are approximately ten times the amount of bacterial cells living in our gastrointestinal (GI) tract alone (stomach and intestines) than there are cells which make up our bodies (Conlon & Bird, 2014). That’s a lot of bacteria! But this is not a bad thing. Bacteria (and other microorganisms), contrary to popular belief, offer many advantages to us. One of the best-known bacteria, Escherichia coli (E. coli), lives in our intestines. We share a symbiotic relationship with this species, meaning we offer each other advantages - E. coli get a warm, moist home while they provide us with vitamins, such as vitamin B, and aid in food digestion. It is also believed that the “good” bacteria living inside us prevent the colonization of other microbes which would do us harm by competing for living space (Tlaskalová-Hogenová et al, 2004). See figure 1 for a summary of the different species of bacteria living in the human GI tract.
As figure 1 illustrates, there are approximately two hundred different bacterial
species living in the human mouth. Experiments have shown that tooth decay,
one of the most prevalent chronic diseases of people worldwide, is caused by
bacteria. A number of bacteria living on the crowns or roots of teeth ferment
carbohydrates (sugars) that may remain after meals and produce acids. This
complex reaction leads to dental caries over time (Selwitz et al, 2007). One
such bacteria involved in this process is the lactobacillus species, which
ferments the sugar lactose, found in milk, and produces lactic acid. This
bacteria is also commonly used to produce cheese and yogurt. Another
common human process which can be attributed to bacteria is body odour.
The armpits, or “axilla”, offer a great living environment for certain bacteria
who thrive in the warm and moist conditions and also make use of molecules
contained in human sweat. Experiments have also shown that an
“acidic odour”, caused by the bacteria’s interaction with the sweat, is what
causes the common human body odour rather than the sweat itself
(Leyden et al, 1981).
The study of these microscopic creatures has provided insight into many
important processes, including ones involving human health, which would be
impossible without microbiology. Its importance to society and to our wellbeing
is still being investigated and our understanding continues to grow.
At a structural level, bacteria are single-celled (unicellular) organisms. They possess a single chromosome, on which they carry their DNA – the information required by all cells to carry out their functions. They also have a cell wall – a thick outer layer which protects the cell and holds it together. See figure 2 for an overview of a basic bacterial cell. Similarly to normal human somatic (body) cells, bacteria have a cell membrane surrounding the cell. Different proteins make up a considerable portion of bacterial structure. The proteins and sugars expressed by a bacteria are what determine the strain. For example, E. coli normally lives inside us but one strain in particular causes severe food poisoning. This strain is characterised by specific proteins which make up its structure. One such protein is a flagellar protein, which is involved in the structure of the flagella, a thread-like “tail” which some bacteria possess in order to help them move.
When thought about with respect to size, approximately one thousand bacterial cells would fit into the full stop at the end of this sentence. Bacteria replicate through a process known as binary fission, by which the bacterial
cell simply splits to divide into two. For further information on bacterial
structure, specifically in relation to the mechanism of antibiotics and how
bacteria can become resistant, see the second and third blogs of this series.
Fungi can be both unicellular and multicellular. Examples of multicellular fungi
include mushrooms. These are not considered microorganisms. Yeast is a
well-known example of a fungus. . It is a unicellular microbe and the yeast
Saccharomyces cerevisiae (S. cerevisiae) is commonly used to make alcohol
and baked goods, such as bread. Fungi are the largest type
of microorganism. S. cerevisiae cells are typically 10-15 times larger than
E. coli cells, for example. Fungi, when thought about in terms of human
interaction, are mostly found growing on the skin and can sometimes cause
skin infections. Common areas where various species of fungus grow include
the scalp and feet. Aspergillus niger (A. niger) is one of a few species of fungus which causes the fungal skin infection known as “athlete’s foot”. Most fungi reproduce through spores, which mature fungal cells release into their environment. A good example of this is seen in the species Penicillium notatum (P. notatum), most commonly seen in bread mould. Spores which may be floating in the air can land on bread and lead to the growth of the mould. Most fungal cells have a tubular structure, such as A. niger and P. notatum. However, S. cerevisiae cells are basic round cells.
Viruses are smaller than bacteria and fungi. Their general structure consists of a protein coat (“capsid”) surrounding a single piece of DNA or RNA, which codes for proteins essential to their survival/replication. Viruses cannot survive without a host. This is a major difference between them and other microorganisms. It is also one of the reasons why viruses are not considered as “living”. Without viable hosts, viruses could not replicate and would die. The flu, for example, is caused by the influenza virus and is spread from person to person through saliva or droplets from sneezing, coughing, etc. These can carry the virus into a new host by entering the eyes, nose or mouth. The virus, like all other viruses, invades host cells, injecting its own DNA (or, in the case of influenza, RNA) into host cells and using them as sites of replication. The host cell is used like a machine, to make everything required by the invading virus. This is done until the cell fills up with newly-replicated viral cells, which are released into the surrounding environment, killing the host cell, ready to invade more cells.
As previously mentioned, differences in structure of some microorganisms lead to different strains. There are different strains of influenza virus also, characterized by surface proteins on the viral capsid, namely hemagglutinin and neuraminidase. Mutations can come about which cause the constant changing of virus ultrastructure. This is the fundamental reason why we get the flu more than once. If there was just one strain of influenza virus, which never changed/mutated, we would become immune to that virus after getting the flu once, or after receiving a vaccination. The next time we came in contact with it, our immune system would be able to detect and deal with it quickly and effectively.
Viruses offer a number of advantages (although significantly less than other microbes!). One such advantage is offered by the bacteriophage, a particular type of virus which infects bacteria. Using bacterial cells as hosts, bacteriophage can lead to the rapid death of certain bacteria. Bacteriophage can now be used to treat poultry, in order to kill the specific strain of E. coli which would cause food poisoning (Monk et al, 2010). Figure 3 shows how some of the microorganisms mentioned above look when viewed using a microscope. These images are included in Microbe Match, a game created for fifth and sixth class students as part of an overall project to promote microbiology and raise awareness about antibiotic resistance (see further blogs). All images online, open-access, through Creative Commons
Berg, R.D. (1996). The indigenous gastrointestinal microflora. Trends in
Microbiology 4, 430–435.
Conlon, M.A., Bird, A.R. (2014). The Impact of Diet and Lifestyle on Gut Microbiota
and Human Health. Nutrients 7, 17.
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Leyden, J.J., McGinley, K.J., Holzle, E., Labows, J.N., Kligman, A.M. (1981). The Microbiology of the Human Axilla and Its Relationship to Axillary Odor. J Investig Dermatol 77, 413–416.
Monk, A.B., Rees, C.D., Barrow, P., Hagens, S., Harper, D.R., 2010. Bacteriophage applications: where are we now? Bacteriophage applications. Letters in Applied Microbiology 51, 363–369.
Selwitz, R.H., Ismail, A.I., Pitts, N.B. (2007). Dental caries. The Lancet 369, 51–59.
Tlaskalová-Hogenová, H., Štěpánková, R., Hudcovic, T., Tučková, L., Cukrowska, B., Lodinová-Žádnı́ková, R., Kozáková, H., Rossmann, P., Bártová, J., Sokol, D., Funda, D.P., Borovská, D., Řeháková, Z., Šinkora, J., Hofman, J., Drastich, P., Kokešová, A. (2004). Commensal bacteria (normal microflora), mucosal immunity and chronic inflammatory and autoimmune diseases. Immunology Letters 93, 97–108.
by Sinead Woods
Do you want the good or the bad news first?
The Irish Times published an article on Thursday the 19th of November which read ‘Superbug breaches final antibiotic line of defence’ (The Irish Times, 2015). What is ironic about this particular publishing date is that it falls within the World Health Organisations (WHO) first Antibiotic Awareness Week. Antibiotic Awareness Week is designed to raise much needed awareness for the global health problem that is Antibiotic Resistance – the findings in this article described all too well the need for a greater understanding of this problem. In an announcement in the Journal Lancet Infectious Diseases researchers from China, Britain and the US declared that they have identifies a new form of resistance. But what makes this resistant strain any different to the many other superbug e.g. Methicillin-resistant Staphylococcus aureus (MRSA). Researchers are walking on new ground as they have discovered resistant strains to the drug colistin the drug used when all else is failing. These findings suggest that we have entered the post antibiotic era and that Antibiotic Resistance is no longer a predicted threat for the future, antibiotic resistance is the here and the now! (Who.int, 2015).
The Rules of Combat
For Your Information?
Antibiotics only treat bacterial infection therefore will not work on colds, flu's and some coughs
Skipping days and finishing your course of antibiotics early means you have not killed all the bacteria ad so you may need more antibiotics to kill off the infection but you may also be promoting the growth of resistant bacteria.
You should never save antibiotics for later as they may not be the correct antibiotic for your infection but also there would not be enough antibiotics to complete the full course of treatment.
Similarly antibiotics that are shared may not be the correct antibiotic and there would not be enough antibiotics to complete the full prescription.
As discussed in the Antibiotics blog antibiotics originate from other microorganisms. Therefore it is no surprise that the search for new antibiotics has focused on microorganisms but not just any microorganisms, soil microbes. Soil microbes produce a variety of substances which possess the ability to kill each other. In other words the microbes are having an ongoing civil war of a chemical nature! However, until recently only about 1% of soil bacteria could be cultured in the lab and so their chemical weapons were untouchable.
Last year German and American scientists developed an innovative piece of technology which led to the discovery of teixobactin (Ling et al., 2015). Teixobactin is a substance which is believed to have the potential to become the first new antibiotic since 1987! It acts by disrupting the cell membrane of some bacteria. But what makes teixobactin so special? Teixobactin has been found to have the ability to destroy some of the most resistant bacterial strains known, such as MRSA. It also has the added benefit of having a very low potential for the development of resistance. The innovative method which ultimately led to the discovery of teixobactin is also very interesting. The researchers involve developed a new assay which screens for possible antibiotic compounds which they called iChip. As already mentioned the search for antibiotic compounds from soil microbes has been the focus since the late 1980’s. iChip is capable of culturing a whopping 99% of soil bacteria – the other 1% can be cultured in the lab. The chip is made up of hundreds of small chambers which contain soil. These chambers allow the bacteria to be cultured in their optimal environment. The cultured bacteria are then overlaid with a gel containing Staphylococcus aureus or Mycobacterium tuberculosis- both are majors causes of infections in humans. If a bacterial colony fails to grow over one of the chambers than the bacteria within the chamber may be producing an antibiotic. Over 10,000 bacteria have been screened by the iChip and one such discovery has been Teixobactin. The iChip technique has the potential to lead to many new antibiotics in the future. Teixobactin is still, however, in pre-clinical trials. It has yet to be tested on animals and humans. Fingers crossed that it makes it through the other side.
The results could be plentiful
Slow and Steady wins the race?
Scientific researchers are competing moderately well in a race with what can only be described as strong competitors. Will the new and old antibiotics get the much needed approval, will the answers lie in the plants or soil. Time will only tell.
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The Irish Times, (2015). Superbugs breach final antibiotic line of defence. [online] Available at: [Accessed 20 Nov. 2015].
Who.int, (2015). WHO | WHO’s first global report on antibiotic resistance reveals serious, worldwide threat to public health. [online] Available at: [Accessed 20 Nov. 2015].
Figure 1: World Health Organization, (2015). World Antibiotic Awareness Week. [online] Available at: [Accessed 29 Nov. 2015].
Figure 2: Tyllerblack.wikispaces.com, (2015). tyllerblack - Science Lab 101. [online] Available at: [Accessed 29 Nov. 2015].
Figure 3: Ramsscience.wikispaces.com, (2015). ramsscience - Streptococcus Pneumonia. [online] Available at: [Accessed 29 Nov. 2015].
Figure 4: Globalganjareport.com, (2015). labor. [online] Available at: [Accessed 29 Nov. 2015].
So maybe all the information above was all just bad news but unfortunately that is the nature of the resistant beas.Scientists have been ‘Racing Resistance’ since Alexander Fleming discovered antibiotics in 1928 (for more info on the discovery of antibiotics refer to the antibiotics blog). But science is not giving up without a fight against resistant bacteria. Researchers have tactics of their own to combat resistance but before they are discussed it is important to understand that the general public have a role to play in this combat.
Play your part in combating antibiotic resistant bacteria by following the instructions on the antibiotic label. Taking antibiotics properly and responsibly will provide the scientific researchers the time they so desperately require to discover new antibiotics. Take a look at the Battling Bacteria resources created to teach 6th class about Antibiotics and Antibiotic Resistance. No new antibiotics have been approved by the FDA in the last 30 years but scientists are searching high and low for a breakthrough.
Unfortunately, we cannot wait to see if teixobactin or any of the other antibiotics receive approval. Instead we must alter existing drugs in the hope to treat highly-resistant bacteria. Many scientists are therefore focusing their research efforts on the redesign of old, discarded antibiotics in the hope of increasing their stability and effectiveness. Theses antibiotics were originally abandoned as they were only effective on a small number of bacteria. A team of scientists led by St. Jude Children's Research Hospital have changed the chemical structure of an old antibiotic called spectinomycin. (Lant, 2015) Spectinomycin is a 1960’s antibiotic and although it is safe it is known to be weak which makes it the perfect candidate for a design makeover. The team involved created new ‘variations’ of spectinomycin which were made more potent. The results showed that one of the new and improved spectinomycin was as effective protecting against Streptococcus pneumonia as ampicillin in mice studies.
Prof. Gibbons of University College London is involved in another interesting area of antibiotic research- the natural antibiotic effects of a variety of plants and it just so happens that one of the most promising is the cannabis plant (Appendino et al., 2008). In 2008, Prof. Gibbons and his colleague Prof. Appendino demonstrated the ability of Cannabinoids (chemicals extracted from marijuana) to fight MRSA. The researchers did so by testing the chemicals on six strains of MRSA and it was found that the plant extracts were as effective at killing the bacteria as commonly prescribed antibiotics. Surprisingly it was then discovered that cannabinoids were as effective at killing bacteria as vancomycin. Not surprisingly however antibiotic cannabis extracts have yet to be FDA approved as they have not undergone animal or human studies.