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Category: Microbiology

Measles vaccine hesitancy leads to outbreaks, deaths of unvaccinated

Many people are afraid of getting measles vaccine these days. The fear arises from the allegedly adverse effects of it, such as autism. However, this fear comes along with the resurgence of the dreaded measles outbreak. Consequently, measles once again takes many lives, especially of the children, who ought not die from such a preventable disease.




Measles vaccine being linked to autism

In 1998, a team of scientists headed by Andrew Wakefield published a paper in refutable science journals. Accordingly, MMR vaccine — a cocktail of vaccine that protects against measles, mumps, and rubella— seems to have a causal link to autism in children.[1] He and his colleagues reported twelve children that displayed delay in growth development; eight of them had autism a month following MMR vaccine. However, the paper was later retracted. Accordingly, “several elements” of a 1998 paper Lancet1998;351[9103]:637–41 “are incorrect, contrary to the findings of an earlier investigation”[2]. The retraction clearly indicated data misconception. However, that did not end there. Wakefield and his team published yet another study. Again, they implicated measles virus to autism.




Second study, still questionable

In 2002, Wakefield and his team biopsied samples from the intestines of two groups of children: with autism and control (without autism). They tested the presence of measles virus genome via reverse-transcriptase PCR and in situ hybridization. They reported 75 of 91 children with autism tested positive for measles virus genome. In the control group, only five of 70 were positive.[3]  Accordingly, their findings corresponded to their earlier conjecture linking measles virus to autism in children. However, critics still found critical flaws.[4] For instance, the authors failed to stipulate with proof the origin of the measles virus genome in the patients — whether from nature or from the vaccine.




Studies refuting the link

Two independent large-scale studies (one in California, USA and another in England, UK) denied the link between MMR vaccine and autism. Truly, the number of children with autism dramatically increased. However, the percentage of children receiving MMR vaccine remained constant. The empirical data on a larger scale of population indicated the absence of causal relationship between measles vaccine and autism.[4]





The side effects associated with MMR vaccine are mild symptoms of measles, mumps, and rubella. And not all children administered with it will show symptoms. As for measles, the common symptoms include swelling and redness at the site of injection, fever, and rash. Rare symptoms include anaphylaxis, bruise-like spots, and fits.[5] No categorical study has fully established that MMR vaccine causes autism in children. Nevertheless, many people remain hesitant despite the many years of proven efficacy of measles vaccine. Their worries were aggravated by the likes of Wakefield studies linking MMR vaccine to autism in children.


Dubbed as anti-vaxxers, these people utterly lost their confidence on vaccines so much that they secluded and kept their children from getting vaccinated. The main reason arises from their fear that vaccines would cause more harm than good. Some of them even took a legal step against vaccine manufacturers for allegedly having identified the culprit of their child’s developmental delay. And despite the disavowal of Wakefield’s paper and having been repudiated by ensuing studies dissociating autism from MMR vaccine, many people including autism advocacy groups have not abandoned their skepticism. Some of them even came up with a “conspiracy theory” that vaccine manufacturers may be conspired into hiding the “truth”, i.e. MMR vaccine causes autism.[2]




Pathobiology of measles

The genus Morbillivirus, a single-stranded, negative-sense RNA virus, is the causative agent of measles, the highly contagious airborne disease. Humans are the only known host of the virus. The video below describes how the measles virus infects the host cell.


[Video credit: Folks from Osmosis, Doc James; Source: Wikipedia, CC-BY-SA 4.0 ]


In summary,  the virus infects the epithelial cells lining the trachea or the bronchi upon reaching the mucosa. The virus gains entry into the host cell via its surface protein, hemagglutinin (H protein). The H-protein binds to the receptor (e.g. CD46, CD150, or nectin-4) on the surface of the target host cell. After binding, the virus fuses with the cell membrane to get inside the cell. Then, it makes use of the cell’s RNA polymerase to transcribe its RNA into mRNA strand. After which, the mRNA is translated into viral proteins in which the host cell’s lipid will envelope them for their subsequent release outside the cell. They spread to lymph nodes,  and then to other tissues (e.g. brain and intestines).[6] Soon, the disease manifests as fever, cough, runny nose, inflamed eyes, and rash. Common complications include pneumonia, seizures, encephalitis, and subacute sclerosing panencephalitis.




Measles vaccine


A child getting measles vaccine during the launch of a campaign to immunize children at the Beerta Muuri Camp for internally displaced persons in Baidoa, Somalia on April 24, 2017.

[Credit: UN Photo. Credit: UNSOM Somalia, Flickr]


The vaccine that prevented the disease was first made available in 1963. It may be administered solely or in combinations, like in MMR vaccine. MMR vaccine renders protection against measles, mumps, and rubella viruses. The World Health Organization (WHO) recommends that measles vaccine be administered to infants at nine or twelve months of age. A person needs only two doses during childhood for lifelong immunity.




How vaccines work

Measles vaccine contains live but weakened strain of measles virus. Vaccines work by triggering an immune response from the white blood cells. These cells recognize them through the surface proteins of the virus. White blood cells, such as B cells, produce multifarious antibodies. One of the antibodies can fit to the surface protein. This will trigger the B cell to produce clones, called memory B cells, which, in turn, will produce large amounts of antibodies specific to the identified pathogen.


A re-encounter with the virus having the same surface protein would enable the antibodies to respond quickly by binding with and disabling the virus. They can also make it “palatable” to macrophages and other phagocytic cells that engulf and kill pathogens. How come the measles vaccine remain effective for so many years? The surface proteins of the measles virus are not prone to changes as presumed, and any mutation on them may render them dysfunctional.[7] Thus,  the immune system will always recognize the measles virus. And the immune response would be so quick that most of the time the vaccinated individual would no longer be ill.



Herd immunity

One of the benefits of a rabid immunization program is that the immune protection extends to those who have not received the vaccine yet. Referred to as herd immunity, the community becomes protected from measles when a huge percentage of the population got the vaccine. In a study published in the journal Frontiers in Public Health, measles vaccination in a sequence recommended by WHO apparently helped reduce child mortality.[8] But in order to prevent and ultimately eliminate measles, WHO seeks global immunization coverage of at least 95%.[9]




Recent measles outbreak


The Philippines, especially the NCR, currently experiences a large measles outbreak. CDC’s Jim Goodson took this photo of a child stricken with the disease during his visit in Manila to respond to the outbreak.

[Credit: CDC Global, Flicker, CC BY-SA 2.0]


Failure to reach the idyllic 95% global coverage leads to the inevitable measles outbreak. For several years, global coverage with the first dose of measles vaccine has stood at only 85% whereas the second dose, at 67%. Thus, measles outbreaks occurred in all regions with over a hundred thousands of fatalities mainly due to serious complications. In 2000, about 21 millions of lives have been saved due to measles vaccine. However, measles cases around the globe surged by more than 30% from 2016.[9]


Dr. Seth Berkley of Gavi, the Vaccine Alliance, elucidated the reasons of the alarming resurgence of measles of recent. He said, “Complacency about the disease and the spread of falsehoods about the vaccine in Europe, a collapsing health system in Venezuela and pockets of fragility and low immunization coverage in Africa are combining to bring about a global resurgence of measles after years of progress. Existing strategies need to change: more effort needs to go into increasing routine immunization coverage and strengthening health systems. Otherwise we will continue chasing one outbreak after another.”[9]




Concluding remarks

Measles vaccine has indubitably protected millions of lives. However, because of the escalating apprehensions and the reluctance towards measles vaccination, we fell short from achieving the goal of eliminating the disease. If only we could stick by the goal and support local immunization program efforts, we might have already won it over once and for all.  Measles is a preventable disease and measles vaccine has already been tried and tested for over so many years. I hope it would not reach to the point whereby an immunization mandate would be the inevitable recourse when in essence we can simply heed the call.




— written by Maria Victoria Gonzaga





1 Wakefield, A.J., Murch, S.H., Anthony, A., et al. (1998). Ileal-lymphoid-nodular hyperplasia, nonspecific colitis, and pervasive developmental disorder in children. Lancet, 351: 637-641.

2  Eggertson, L. (2010). Lancet retracts 12-year-old article linking autism to MMR vaccines. Canadian Medical Association Journal182(4), E199–E200. [Link]

3 Uhlmann, V., et al. Potential viral pathogenic mechanism for new variant inflammatory bowel disease. Journal of Clinical Pathology: Molecular Pathology 55:1-6, 2002. [Link]

4 Offit, P.A. (n.d.). Vaccines and Autism. [PDF]

5 NHS Choices. (2019). Vaccinations. Retrieved from [Link]

6 Moss, W.J. & Griffin, D.E. (14 January 2012). “Measles”. Lancet379 (9811): 153–64. [doi:Link]

7 Cell Press. (2015, May 21). Why you need one vaccine for measles and many for the flu. ScienceDaily. Retrieved from [Link]

8 Frontiers. (2018, February 12). Measles vaccine increases child survival beyond protecting against measles: New study shows all-cause mortality is significantly lower when a child’s most recent immunization is a measles vaccine. ScienceDaily. Retrieved from [Link]

9 World Health Organization. (2018, November 29). Measles cases spike globally due to gaps in vaccination coverage. Retrieved from [Link]

Lurking beneath the ice

Scientists found dead tardigrades beneath the Antarctica based on their report published of recent.[1] It was a surprising discovery since tardigrades have acquired the mark as the tiny infinities. They are so resistant to extreme conditions that they are thought of as some sort of “immortals“. Nonetheless, scientists found remains of tardigrades, together with crustaceans in deep, frozen Antarctic lake.[1]



Antarctic Realm – The Cold Realm


Antarctic realm
The Antarctic biogeographic realm – the smallest of all realms.


The Antarctic is a region located in the southern-most tip of the Earth. The biogeographic realm that includes the Antarctic is called the Antarctic realm. A biogeographic realm refers to an area of land where similar organisms thrived and then evolved through periods of time in relative isolation.[2] It rouses extensive research with the paramount objective of understanding the extent of biodiversity, especially the distributional patterns of residing organisms and the biological evolutionary history incurred.



The Antarctic biogeographic realm is the smallest of all realms. It spans a total area of about 0.12 million square miles. Its components include the land area, the Antarctic tectonic plate, the ice in the waters, and the ocean itself. [2]  Because of the cold temperature, few floral species are able to persist and thrive. At present, around 250 lichens, 100 mosses, 25-30 livertworts, 700 algal species, and two flowering plant species (i.e. Antarctic hair grass and Antarctic pearlwort) inhabit the region. As for fauna, animal species include the penguinsseals, and whales.[2]



An Icy Surprise


Tardigrades . [Credit: Willow Gabriel, Goldstein Lab –]

The discovery of the remains of tardigrades was unexpected, according to David Harnwood, a micropaleontologist. Late last year, Harnwood and his research team drilled a hole in the subglacial Lake Mercer. This frozen lake had been undisturbed for millennia.  Thus, their research project SALSA (Subglacial Antarctic Lakes Scientific Access) was the first to conduct direct sampling. They were absolutely surprised to find these water bears –frozen and dead.


Astounded, the animal ecologist, Byron Adams, conjectured that these tardigrades might have come from the Transantarctic Mountains, and then carried down to Lake Mercer. [1] Further, he said, “What was sort of stunning about the stuff from Lake Mercer is it’s not super, super-old. They’ve not been dead that long.”



Chilly Giants

“Mollivirus sibericum” found in Siberian permafrost.
[Credit: © IGS CNRS/AMU]

In September 2015, Jean-Michel Claverie and others reported two giant viruses (i.e. ”Pithovirus sibericum” and ”Mollivirus sibericum”) that they revived from a 30,000-year-old permafrost in Siberia.[3,5] Once revived, the viruses quickly became infectious to their natural hosts, the amoebae. [5] Luckily, these chilly giants do not prefer humans as hosts. Nonetheless, the melting of these frozen habitats could implicate danger to the public health when pathogens that can infect humans escape the icy trap.



A frozen Pandora’s Box

The frozen regions of the Earth hold so many astonishing surprises waiting to be “thawed”. In August 2016, a 12-year old boy from the Yamalo-Nenets region of Siberia died from anthrax. Reports included a few number of locals and thousands of grazing reindeer as well.[6] Prior to the anthrax outbreak, a summer heatwave caused the melting of the permafrost in the Yamal Peninsula in the Arctic Circle. The thawing of the frozen soil unleashed anthrax bacteria presumed to have come from the carcass of their reindeer host that died over 75 years ago. Their release apparently reached the nearby soil, water, the food supply, and eventually their new hosts.[5] The anthrax bacteria survived because they form spores that can protect them during their dormancy.




A Hotter Earth

Global warming supposedly increases the average temperature of the Earth’s surface enough to cause climate change. Accordingly, the global surface temperature increased 0.74 ± 0.18 °C (1.33 ± 0.32 °F) during the last century. The temperature rise brings threat as it could lead to environmental changes that could cause adverse effects of massive magnitude. One of which is the destruction of habitats due to the subsequent rise of water level from the melting of ice. Deadly pathogens could rise again from their cold slumber and plausibly cause another major mass extinction in no time. So, while we try to explore the deeper mysteries lurking beneath the ice, we should also make sure that we remain a step ahead. Claverie[5] excellently put it:

The possibility that we could catch a virus from a long-extinct Neanderthal suggests that the idea that a virus could be ‘eradicated’ from the planet is wrong, and gives us a false sense of security. This is why stocks of vaccine should be kept, just in case.



— written by Maria Victoria Gonzaga





1  Berman, R. (2019, January 18). Dead – yes, dead – tardigrade found beneath Antarctica. Retrieved from [link]

2  Pariona, A. (2018, May 18). What Are The Eight Biogeographic Realms? Retrieved from [link]

3 CNRS. (2015, September 9). New giant virus discovered in Siberia’s permafrost. ScienceDaily. Retrieved from [link]

4  ‌ Wikipedia Contributors. (2018, November 10). Antarctic realm. Retrieved from [link]

5  Fox-Skelly, J. (2017, January 1). There are diseases hidden in ice, and they are waking up. Retrieved from [link]

6  Russia anthrax outbreak affects dozens in north Siberia. (2016, August 2). BBC News. Retrieved from [link]

7  Biology-Online Editors. (2014, May 12). Biology Online. Retrieved from [link]

“Mutualism factor” could explain why body does not attack normal flora

When sadness reeks in and you feel as if you are all by yourself, think again. That is because you are never alone. As a matter of fact, millions of microorganisms reside in our body day in and out. They are the normal flora. Our body is a world of microscopic living entities that inhabit our body without essentially causing a disease. Rather, they live in us in harmonious mutualism. Thus, our body is not ours alone. Hence, we can say we are not absolutely sterile from the moment we are born.




Normal flora

Typically, the body has about 1013 cells and harbors about 1014 bacteria.1 The multifarious yet specific genera of bacteria that predominate the body is referred to as the normal flora. In essence, the normal flora thrives in a host in a mutualistic lifestyle. The microbes take advantage from living stably in the body. In return, they confer benefits to the human host. For instance, their presence helps prevent other more harmful microbes from colonizing the host. Some of them biosynthesize products that the human body can use. Nevertheless, an immunocompromised host could suffer in cases when these bacteria became overwhelming in number, and thereby cause detectable harm, like infections or diseases.




Normal flora in the gut

normal flora in the gut
Escherichia coli, one of the many bacterial species of the normal flora in the human gut


Microbes that normally thrive in the gut are greater in density and diversity compared with those in other body parts. Nevertheless, they vary in density depending on the location in the gastrointestinal tract. For instance, the stomach harbors about 103 to 106/g of contents whereas the large bowel of the large intestine has about 109 to 1011/g of contents. The normal flora in the stomach has fewer normal microbial inhabitants due to its acidity. The ileum of the small intestine contains a moderate microbial number, i.e. 106 to 108/g of contents.1


Some of the various bacterial species of the normal gut flora includes the anaerobes, Enterococcus sp., Escherichia coli, Klebsiella sp., Lactobacillus sp., Candida sp., Streptococcus anginosus and other Streptococcus sp.. Some of these bacteria aid in the production of bile acid, vitamin K, and ammonia since they possess the necessary enzymes.





Certain normal gut bacteria can become pathogenic. They could cause a disease when opportunity presents such as when changes in their microbiota favor their growth. Be that as it may, a healthy individual would not be usually harmed by their presence. Thus, question arises — why our immune armies do not, by and large, act against the normal flora as aggressively as they would in the presence of more harmful pathogens.


Karen Guillemin, a professor of biology and one of the authors of a paper that appeared in a special edition of the journal eLife, was quoted3: “One of the major questions about how we coexist with our microbial inhabitants is why we don’t have a massive inflammatory response to the trillions of the bacteria inhabiting our guts.




“Mutualism factor”

Guillemin and her team of scientists reported that they uncovered a novel anti-inflammatory bacterial protein they referred to as Aeromonas immune modulator (AimA).  Accordingly, AimA is a protein produced by a common gut bacterium, Aeromonas sp., in the animal model, zebrafish.  The researchers found that AimA alleviated intestinal inflammation and extended the lifespan of the zebrafish from septic shock.2 Furthermore, they described it as an immune modulator that confers benefits to both bacteria and the zebrafish host.


The newly-discovered protein seems to be the first of its kind. Nevertheless, it is structurally similar to lipocalins, a class of proteins that, in humans, modulate inflammation. Based on their findings, the removal of this protein caused more intestinal inflammation in the host and the destruction of the normal Aeromonas gut bacterium. The reintroduction of AimA reverted to “normal”, i.e. the host, relieved from inflammation and Aeromonas’ typical density, restored. AimA appears to represent a new set of bacterial effector proteins. And, Guillemin referred to them as mutualism factors.3


Guillemin and her team postulate that many more of these mutualism factors exist even in humans, and yet to be found. These mutualism factors may have therapeutic potential for use in modulating inflammation especially in medical conditions such as sepsis and certain metabolic syndromes.




— written by Maria Victoria Gonzaga





1 Davis, C. P. (1996). Normal Flora. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston. Retrieved from [link]

2 Rolig, A. S., Sweeney, E. G., Kaye, L.E., DeSantis, M. D., Perkins, A., Banse, A. V., Hamilton, M.K., & Guillemin, K. (2018). A bacterial immunomodulatory protein with lipocalin-like domains facilitates host–bacteria mutualism in larval zebrafish. eLife. [link]

3 University of Oregon. (2018, November 6). Novel anti-inflammatory bacterial protein discovered: Newly discovered protein alleviates intestinal inflammation and septic shock in an animal model. ScienceDaily. Retrieved from [link]

Porphyromonas gingivalis: Periodontitis bacterium induces memory impairment and neuroinflammation

Porphyromonas gingivalis is a bacterium commonly associated in periodontitis a chronic inflammatory disease in the oral cavity.  Periodontium is composed of periodontal ligament, cementum, alveolar bone and gingiva. Porphyromonas gingivalis is a gram-negative bacterium that contains toxic components. It is characterized by the presence of edema and destruction of tissue supporting the teeth. In which periodontal bacteria enters into circulation that leads to bacteremia and system dissemination of bacterial products. Moreover, Porphyromonas gingivalis can promotes systemic effects through expression of inflammatory mediators like pro-inflammatory cytokines. As a consequence it is confirmed to be associated with systemic diseases such as diabetes, respiratory disease and cardiovascular disease.

Potential effects of Porphyromonas gingivalis

Neurodegenerative diseases have been recognized as the major cause of cognitive and behavioral damage. It is known that peripheral infections could activate microglial cells within the nervous system enhancing development of neurodegeneration. Thus, the inflammatory molecules in the brain could be enhanced by periodontitis that increase inflammatory levels promoting the development of Alzheimer’s disease. In this particular research Porphyromonas gingivalis infection may impair cognition by elevating expression of pro-inflammatory cytokines. It is also shown that the infected mice displayed impaired memory and learning abilities. Elevated levels of pro-inflammatory mediators in the blood can lead to direct or indirect transport to the brain.


Periodontal infection caused by Porphyromonas gingivalis promotes neuro-inflammatory response via releasing pro-inflammatory cytokines. In which inflammation induces alterations in neurovascular functions causing increased in blood brain barrier permeability and aggregation of toxins. In brain trauma, infection and presence of endogenic abnormal protein aggregates can activate secretions of TNF-α. That plays a pivotal role in the development and functions of central nervous system. Moreover, aging is also associated to chronic inflammation which exerts additional stress to the brain nerve cells. Additionally, during systemic inflammation the functions of the blood-cerebrospinal fluid barrier were also significantly affected.


Therefore, Porphyromonas gingivalis periodontal infection may induce age-dependent brain inflammation. Also periodontitis can cause memory impairment which has a similar effect on the development of Alzheimer’s disease. Furthermore, aging is the major risk factor of Alzheimer’s disease and is correlated with elevated glial responsiveness. And in due course might increase the brain’s susceptibility to injury and disease.


Source: Prepared by Joan Tura from BMC Immunity and Aging

Volume 15:6, January 30, 2018


Role of selenium-fortified yogurt against aflatoxin-contaminated nuts

Aflatoxins produced by a certain molds that are poisonous carcinogens which grow mostly in soil, hay, decaying plants and grains. It can affect livestock and human as natural contaminants in foods like peanuts and corn meal. There are four types of aflatoxins these are B1, B2, G1 and G2 in which all are teratogenic, carcinogenic and immunosuppressive. Its toxic effect might be due to the generation of free radicals resulting into lipid peroxidation that damage biological system. On the other hand yogurt is produced from the bacterial fermentation of milk. In which bacteria produces lactic acid that acts on milk protein to give yogurt its texture and tart flavor. However, yogurt contains plenty of probiotic bacteria that offer benefits as microflora in the intestines. It also helps boost immune response and suppress carcinogenesis since fermented dairy products contain live lactic acid bacteria.


Selenium-fortified yogurt protects against aflatoxin toxicity

Yogurt has been known as therapeutic to various disorders including lactose intolerance, indigestion, intoxication, gastroenteritis, kidney, liver disorders and cancer. Selenium added to yogurt considered as the basic trace elements vital for normal growth and development in humans and animals. It also acts as anti-oxidant as well as improves nutritional values. Additionally, selenium has both enzymatic and structural functions that protect harmful reactive oxygen and minimized the production of hydrogen peroxide from aflatoxins. Ingestion of aflatoxins leads to weight loss due to the change in digestive enzymes activity that causes malabsorption of nutrients.


Aflatoxins will impair the biosynthesis of protein which results to the degranulation of the endoplasmic reticulum. It also caused liver fibrosis and poses health risk to humans and livestock. In this research , a positive results shows that selenium-fortified yogurt suppress the level of aflatoxins in rats. It also proved that with selenium contents inhibit the activity of enzymes related to carcinogenesis. Since yogurt improves intestinal mucosa and microflora that influence intestinal barrier. These yogurt bacteria inhibit the peroxidation of lipids by foraging reactive oxygen.


Therefore, consumption of nuts infected with aflatoxins caused toxicity mainly at the kidney and liver. But intake of selenium-fortified yogurt can definitely suppress against aflatoxins toxicity. In general, application of probiotic bacteria and selenium is vital and viable therapeutic approach to improve safety in food industry. Indeed, it is recommended to eat fresh nuts to avoid aflatoxins along with selenium-fortified yogurt to lessen its toxicity.


Source: Prepared by Joan Tura from BMC Agriculture and Food Security

Volume 7:21, June 2018



First Video Proof That Could Explain Antibiotic-Resistant Superbug Bacteria

Amidst the battle for supremacy, our army of immune cells relentlessly wages war against various pathogens, especially superbug bacteria. Despite the pool of ample winnings, our body still experiences defeat from time to time. We succumb to diseases as the war reels its favor towards the tenacious pathogens. Of course, we cannot allow our immune defense to be utterly defeated. Otherwise, we’d be dead. As bacteria advance by taking over much space and nutrients inside our body, we get external help through antimicrobial chemicals that scientists continue to contrive.  Unfortunately, antibiotic resistance has surfaced and turned certain strains of bacteria into a superbug – one that has become resistant to the effects of antibiotics.




Chemical warfare prior to the rise of a superbug

Antimicrobial chemicals, particularly antibiotics, came into existence as chemicals that were strategically designed and produced with the intent of killing pesky bacteria. In 1928, penicillin was discovered, which led to its use as the first natural antibiotic capable of undermining a spectrum of bacteria, if not by killing, by inhibiting their growth. Its role as a wonder drug against various bacteria caused Alexander Fleming to receive a duly recognition by winning a Nobel prize award for its discovery. Soon, more antibacterial agents came up to our defense. Antibiotics, such as penicillin and cephalosporin, destroy bacterial cell wall whereas polymyxins target bacterial cell membrane. Rifamycin, quinolones, sulfonamides, and the likes interfere with the enzymes essential to bacteria. Once again, we gained an upper hand.




Bacteria resisting: the rise of a superbug

A Scanning Electron Microscope (SEM) image of cells of the bacteria Vibrio tasmaniensis(Credit: Lewis Lab at Northeastern University. Image created by Anthony D’Onofrio, William H. Fowle, Eric J. Stewart and Kim Lewis)


While we thought we finally came up with a powerful weapon, the bacteria conjured up an amazing strategy to work in their favour — antibiotic resistance. Some of them started to morph. They evolved and mutated into new strains referred to as superbug. They became capable of resisting the drugs’ antimicrobial effects. One of their strategies is to produce β-lactamases that destroy the structure of β-lactam antibiotics (e.g. penicillin and cephalosporin). The bacteria that evolved into superbug organisms did not just live; they thrived. They multiplied and passed on to the next generation the features that could withstand a number of antibiotics.




DNA uptake by superbug bacteria

Apart from the vertical gene transfer of genes, antibiotic resistance could also be transferred through horizontal gene transfer. It is a mechanism whereby genes are taken up or transposed from one species to another, and one of the possible explanations for the rise of superbug bacteria. DNA uptake by a bacterial cell was captured for the first time in a video by a team of scientists from Indiana University. In the video1, it shows how a bacterial cell takes up DNA fragments from dead bacterial cells through its pilus. Like a harpoon, the pilus was used by the bacterium, Vibrio cholera, to catch and reel a stray DNA fragment, and then bring it inside the bacterial cell via the same pore on its cell wall. It, then, incorporates the DNA into its own genome. Accordingly, this is probably one of the mechanisms for a bacterium to turn into a superbug.

First video evidence of DNA uptake by Vibrio cholera.
(Video credit: Ankur Dalia, Indiana University, uploaded on YouTube by Group IU Biology News)


A researcher from the team, Courtney Ellison, recounted, “The size of the hole in the outer membrane is almost the exact width of a DNA helix bent in half… If there weren’t a pilus to guide it, the chance the DNA would hit the pore at just the right angle to pass into the cell is basically zero.” It appears that the pilus takes a crucial role in horizontal gene transfer. If left to chance the DNA fragment would not easily get inside the cell since the pore was too small for it to fit. Through horizontal gene transfer, those that were once sensitive to the antibiotic could later become superbug bacteria as well. As Ankur Dalia, another researcher from the same team, pointed out, “Horizontal gene transfer is an important way that antibiotic resistance moves between bacterial species….” The video that the research team captured for the first time could explain how antibiotic resistance can be acquired from one superbug bacterial species to another.




The battle is far from over. The antibiotic resistance already raised global concerns as it has rendered certain antibiotics ineffective. Pathogenic superbug bacteria have successfully armed themselves with genes that could neutralize antibiotic effects. Fortunately, scientists do not waver in determining the strategies that superbug bacteria exploit.  The recent discovery of the way by which bacteria employ to make them antibiotic-resistant superbug strains could lead to better therapeutic strikes that could counter them, hopefully, with ample success.




— written by Maria Victoria Gonzaga




1 Indiana University. (2018). IU scientists watch bacteria ‘harpoon’ DNA to speed their evolution. Retrieved from

Human leptospirosis cases in Palermo Italy: Rodents and Climate

Leptospirosis is a corkscrew shaped that is known as one of the most widespread bacterial zoonoses in the world. Symptoms range from mild flu to severe multi-organ failure and fatal pulmonary hemorrhagic syndrome. In which the key factors of these diseases are from stray animals, poor sanitation, rodents, heavy rainfall and flooding. Many regions have been increasingly exposed to leptospirosis infection due to climate change, global warming, poverty and high urban density. Rodents are the main animal reservoir in urban settings mainly involved in pathogenic transmission. Moreover, a high prevalence in rodent population occurs in major cities such as in Baltimore, Tokyo and Copenhagen. In Italy sporadic cases of leptospirosis have been often related to river flooding. This study focused on molecular survey of rodents in the city of Palermo, Italy.


Human leptospirosis cases

Two cases in 2009 of leptospirosis in Palermo during spring and fall seasons and there were 22 locations monitored. A rodent is the main reservoir for leptospirosis related to heavy rainfall and flooding in urban streets and riverbanks. During street floods individual were potentially in contact with water contaminated by infected rodent urine. So, the risk of infection is high but because of good hygienic conditions and economic wellness severe symptoms is rare.  It is also possible that periodic exposures to serovars leave the immune competent population more resistant to infection. Other cases also in Northern Italy an elderly woman has a fatal infection after river flooding occurs.


Based on molecular testing leptospirosis are positive in all species of wild rodents living in almost all areas in the city. Mice and rats are the natural source for this pathogenic infection. The main common problem in Palermo, Italy is the urban street floods from heavy rains and waste accumulation. In which the city is represented by almost ten thousand stray dogs feeding on garbage. Previously, a patient was in contact with contaminated water in street flood after violent cloudburst. Waste collection also is one of the problem in Palermo that eventually facilitates the increased of rodent population.


High prevalence of leptospirosis occurs in mild wet climate, flooding of urban streets and socio-economic problems. Other Italian cities has presence of simultaneous risk factors for leptospirosis, and thus, a major concern from this underestimated zoonosis should be considered by public health authorities and clinicians particularly for elderly and immune-compromised individuals. However, severe symptomatic cases are referred to hospitals and the true prevalence of infection is probably not evaluated.


Source: Prepared by Joan Tura from Journal of Infection and Public Health

Volume 11, Issue 2, March–April 2018, Pages 209-214


Epstein-Barr Virus – It’s More Than Just The Kiss

Epstein-Barr virus — the virus causing the kissing disease or mononucleosis — is eyed as a risk factor for contracting seven other major diseases. This is what the research team at Cincinnati Children’s Hospital Medical Center reported. The Epstein-Barr virus is contracted by kissing or by the oral transfer of saliva. Apparently, once the Epstein-Barr virus infects the body it stays there forever.




Epstein-Barr virus and mononucleosis

Epstein-Barr virus illustration. (Credit: Vix Maria, ©


The Epstein-Barr virus belongs to the herpes family, Herpesviridae. It contains DNA that bears 85 genes and is surrounded by a nucleocapsid. Apart from the nucleocapsid, the virus is further bounded by a protein tegument and an outermost layer of a lipid envelope. The envelope has glycoprotein projections, which are crucial for the virus during its infection of the host cell.1 B cells, the immune cells producing antibodies, are ought to destroy them. However, the Epstein-Barr virus can outwit them by a slick mechanism. The virus invades the B cell, reprograms it, and makes it “follow” its “commands”. The virus is known for causing mononucleosis or the kissing disease. The common symptoms include fever, fatigue, sore throat, rash, and swollen lymph nodes, especially in the neck.




Epstein-Barr virus and the seven major diseases

According to the study led by three scientists, John Harley, Leah Kottyan, and Matthew Weirauch, the Epstein-Barr virus infection has been implicated to seven unrelated serious diseases.2 Previous studies by Dr. Harley and his team have already connected Epstein-Barr virus with the increased risk of developing systemic lupus erythematosus years ago. Recently, however, they found that the virus could also augment the risk of developing other serious diseases, such as multiple sclerosis, type 1 diabetes, inflammatory bowel disease, celiac disease, rheumatoid arthritis, and juvenile idiopathic arthritis.3 A person contracting the Epstein-Barr virus has a greater risk of developing them. This is because the virus produces a protein, Epstein–Barr virus nuclear antigen 2 (EBNA-2), that interacts with the human DNA, especially at genetic risk variants. 2 A genetic risk variant pertains to a variant in the DNA genome that has a potential to cause disease(s).




Epstein-Barr virus and future research

Epstein-Barr virus, known for causing kissing disease or mononucleosis, is linked to other serious diseases.


Dr. Harley and his team suspect that the EBNA2 protein from the Epstein-Barr affects a set of transcription factors. Accordingly, what the seven seemingly unrelated diseases share in common is a set of dysfunctional transcription factors, each affected by the EBNA2 protein.2 When the activity of transcription factors deviate from what they are supposed to do, the host cell (such as B cell) would not be able to carry out its normal function. This, in turn, could progress to certain diseases. With their recent finding, Dr. Harley and his team are optimistic that further intensive research could direct to finding better therapies and preventive methods such as vaccines against Epstein-Barr virus infection.




This recent finding suggests that contracting Epstein-Barr virus can lead to multiple diseases apart from mononucleosis. Therefore, this calls for more studies that aim at finding better cures and preventive measures. Currently, there is no vaccine against Epstein-Barr virus; being able to boost our immunity against the virus may help mitigate the risk to many other diseases, such as those mentioned above.




— written by Maria Victoria Gonzaga




1Odumade, O.A., Hogquist, K.A., & Balfour Jr., H.H. (2011). “Progress and Problems in Understanding and Managing Primary Epstein–Barr Virus Infections”. American Society for Microbiology. 24 (1): 193–209. doi:10.1128/CMR.00044-10
2 Harley, J.B., Chen, X., Pujato, M., Miller, D., Maddox, A., Forney, C., Magnusen, A.F., Lynch, A., Chetal, K., Yukawa, M., Barski, A., Salomonis, N., Kaufman, K.M., Kottyan, L.C., & Weirauch, M.T. (2018). “Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity.” Nature Genetics. DOI: 10.1038/s41588-018-0102-3
3 Cincinnati Children’s Hospital Medical Center. (2018). ‘Mono’ Virus Linked to Seven Serious Diseases. Retrieved from

E.coli Outbreak from Romaine Lettuce

Based on new updates about E.coli outbreaks the CDC extends its warning to include all types of romaine lettuce. It avoids consumers to eat romaine lettuce growing from Yuma, Arizona. And discourage the consumer to buy at grocery store unless proven that it is not come from the same region. Mostly the packaging of the romaine lettuce does not indicate the growing regions. So it encourages consumers to throw away the romaine lettuce even if symptoms of E.coli infections did not occur. Restaurant also prevented to serve any salads containing romaine lettuce that came from Yuma, Arizona. Also the retailers not allowed selling any of it that came from the region.


What is E.coli?

E.coli is a gram-negative coliform bacterium that is facultatively anaerobic. It is enteric bacteria not normally thrive in the intestine of animals and human. Most E.coli strains are harmless and part of normal flora in the gut that offers benefits to the host. By producing vitamin K and preventing any pathogenic bacteria through symbiotic relationships. But some of its strain is harmful like E.coli 0157:H7 that cause serious illnesses. Like gastroenteritis, hemorrhagic colitis and urinary tract infections. The usual symptoms and sign of infections include diarrhea, abdominal cramps, vomiting and fever. Most likely children are more susceptible to infections that develop severe illnesses. This E.coli 0157:H7 produced shiga toxin that caused premature destruction of red blood cells which damaged the kidneys.


What went before?

E.coli outbreaks have sickened at least 53 people in 16 states according to the CDC. Last March 13, 2018 reported to have 31 people hospitalized since the onset of the outbreaks. Five people developed kidney failure but no death have been recorded. No recalls have been made because the CDC could not identify the specific grower that is responsible for the outbreaks. But official released a statement for the consumer to throw away all romaine lettuce even if sickness didn’t appear.


The outbreaks dates started from March 22, 2018 to March 31, 2018. On April 10, 2018, 18 more people from 9 states were added to this outbreak. As of April 12, 2018, another 35 people infected of E.coli 0157:H7 have been reported from 11 states. So far, Pennsylvania has the highest cases of infection followed by Idaho. Health officials advice consumers to avoid buying romaine lettuce up to date unless source known not come from Yuma, Arizona. Additionally, more hospitalization has been reported and in past few days more new cases added to CDC investigation.


Source: Prepared by Joan Tura from Center for Disease Control and Prevention

Microbiological Assessment of Honey in México

Honey is a viscous sweet substance produced by bees from the secretions of plant nectars. It is a product from some regions of Mexico as a sugar supplement and for therapeutic purposes. Honey contains fructose and glucose with low level of water activity and high osmotic potential in humidity. In Mexico apiculture contains high economic and social value wherein forty five thousand producers depend on it. That accounts for almost 19 million beehives placing Mexico as the fifth producing and third exporting country in the world. Microbial characteristics of honey are the built-in biota of bees from the nectar of different flowers that kept overtime. This particular research study evaluates the microbial community of honey produced in Mexico.


Microbial Biota of Honey

Microbial contamination of honey occurs during extraction and handling including dust, air, dirt, flowers and digestive tract of honey bees. Microorganisms commonly found include Bacillus spp., Clostridium spp., Corynebacterium spp., Pseudomonas spp. and some bacteria found in sugars and plants. The official standard in Mexico stated that no more than 1000 CFU/g of non-pathogenic bacteria and 100 CFU/g of molds and yeast are acceptable. Since Mexico is one of the main honey producers that comprised at least 86 thousand tons to be exported.


The study reveals that out of 1,920 samples of honey 40.5% exceeded the limits permitted by the regulatory board. For the yeast and molds 18.1% and 17% of the samples showed more than 100 CFU/g respectively. With regard to Clostridium 12% the samples contained more than 100 CFU/g due to the bees contamination, nectar and external sources. There have been observations also that bee gut contains 27% gram positive bacteria including several species of Clostridium. Although honey has high osmolarity and low water activity yet development of microorganisms found on several sources. However, microbial contamination caused by handlers, equipment and crossed contamination can be controlled by standard sanitation and good manufacturing practices.


Since it reveals that over 40% from the samples did not complies specification for the presence of aerobic mesophilic bacteria. It gives emphasis to local producers the proper handling and minimizing the sources of contamination so it can fit the standard. If honey is used for therapeutic purposes better quality is vital and fulfills quality parameters to remove pathogens. Mexican honey of great percentage has been exported that is why maintaining good hygienic practices during manufacturing is very important.


Sources: Prepared by Joan Tura from  Revista Argentina de Microbiología

Volume 50, Issue 1 January–March 2018, Pages 75-80