Art Project

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The diversity of the microbial world is not only astounding, but awe inspiring. Life as we know it would not be possible without this vast microbial community and oxygenating our atmosphere, cycling our nitrogen, and fixing our carbon. These and so many other processes, allow us to inhabit this Earth and continue to thrive. However, there is still the <1% of microbes which are classified as pathogenic to humans. These microbes, do not help our quality of life but rather, can cause disease and death in our populations.

 

Since 2015 the World Health Organization (W.H.O.) publishes a yearly list of pathogens. These pathogens are those which have been identified to pose the greatest public health risk due to their “epidemic potential and for which there are no, or insufficient, countermeasures.’ (World Health Organization, 2018). The pathogens which are the subjects of my portrait collage are those of the 2018 R&D Blueprint List of priority pathogens. (https://www.who.int/blueprint/priority-diseases/en/)

For my art project I have done small portraits of the pathogens listed by the W.H.O.. It should be noted that these are in no particular order. All of these pathogens are in need of further analysis as well as analysis for treatment methods which would be imperative for stalling an outbreak. One should also note that there is a “Disease X’ within this collage. There is no true disease called Disease X, but rather the potential that an as of yet unknown pathogen that could cause widespread disease epidemics is out there. It is my hope that even though my artistic abilities and nudges to 70’s rock bands may not be the best, they can introduce this information to a broader audience. Since not everyone spends their free time looking at the W.H.O. website.

-Samantha Smith

Painting with Microbes

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Samantha Smith F01

Just a wink and a nudge to my favorite book “East of Eden” by John Steinbeck. I have a a pretty cross stitch of this at home, which admittedly looks a lot better. Perhaps I will stick to my day job and leave the microbe painting to those more artistic than myself.

I used the Eosin Methylene Blue Agar plate for this painting, hoping to achieve a stark different in coloration from the two sources I chose. The lettering and the vine were done with Escherichia coli.  This bacteria is gram negative so is not inhibited by the eosin or methylene blue of the medium. It also produced a deep black color with a metallic green sheen as it ferments lactose with strongly acidic end products. (The green sheen is actually quite pretty, though you can’t tell from the photo). The filigree and leaves are colonies of  Enterobacter aerogenes  which is also gram negative. It produces a pink color because it does ferment lactose, but the end products of fermentation are much less acidic than that of  E. coli.

I would like to add that I had a lot of fun in this assignment and seeing the variety of agar art from the ASM Agar Art Contests.

 

New technique provides a better understanding of bacteria evolution

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New technique pinpoints milestones in the evolution of bacteria
Results show bacterial genomes provide “shadow history’ of animal evolution.
Jennifer Chu, MIT News Office February 7, 2019

References

Danielle S. Gruen, J. M. (2019, January). Paleozoic diversification of terrestrial chitin-degrading bacterial lineages. BMC Evolutionary Biology, 19-34. Retrieved from https://bmcevolbiol.biomedcentral.com/articles/10.1186/s12862-019-1357-8

 

—  Summary:  Researchers from MIT have established organism relationships between fungi and bacteria by reviewing the gene for chitinase (an enzyme which helps to break down chitin). Their review of the mutations, and similarities across different species has allowed them to create an evolutionary tree which correlates microbial evolution with fungal evolution. They found that approximately 450 to 350 million years ago, diversification of three separate bacterial groups diversified as the result of gene transfer with a chitinase utilizing fungi. Below is the resulting evolutionary tree with the fungi identified by purple lines and bacteria with blue lines.

(Gruen, et al. 2019)

—  Connections:  This connects with: Microbial evolution, metabolism, and diversification.
Chitinase allows these bacteria to metabolize chitin as an energy source. This allowed diversification of microbes into new niches ones chitin became more prolific in the environment. Gene transfer was said to make it difficult to genomically identify or differentiate bacterial strains, but here the gene transfer has allowed a better understanding.

—  Critical analysis: I found this article very interesting because, most evolutionary trees are based on rRNA sequencing (highly conserved due to form/function). The use of chitinase to correlate evolutionary relationships between fungus and bacteria is interesting. Especially since the origin of chitinase was in a Fungi (a microorganism that doesn’t look like a microorganism) and the gene has been horizontally transferred to bacteria.

The story was very well written and after reading the original journal publication, it was factually and accurately written. The author did as great job in conveying the information to the general population without losing the integrity of the research. I appreciate the writing style and how it helps those (like myself) who aren’t as well versed in the scientific nomenclature, to understand the information and findings from the research.

 

—  Question:  How many other highly conserved coding regions can we isolate and use in this manner? Are enzymes such as chitinase always highly conserved, or is there slight variations in the conformation, allowing it to mutate without ruining the function of the enzyme?

-Samantha Smith

A2 Microbes in the News (P.gingivalis and Alzheimer’s disease)

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Article and Link:

“We may finally know what causes Alzheimer’s–and how to stop it’
By: Debora MacKenzie
Source: NewScientist.com
Date: 24 January 2019

https://www.newscientist.com/article/2191814-we-may-finally-know-what-causes-alzheimers-and-how-to-stop-it/

Summary

Researchers have found that the formation of amyloid and tau proteins which are signs of Alzheimer’s disease, may be a response to bacterial infiltration. One of the major risk factors of Alzheimer’s is the occurrence of gum disease caused by the bacteria Porphyromonas gingivalis.
They have found that P. gingivalis has been found to infect areas of the brain with Alzheimer’s lesions as well as exacerbating the symptoms of Alzheimer’s in mice who have been infected with P. gingivalis as gum disease. Similarly healthy mice (who have not been engineered to have Alzheimer’s) who have been infected with gum disease and the bacteria P. gingivalis, exhibit amyloid plaques, and neural damage similar to that found in Alzheimer’s affected brains.
Enzymes which P. gingivalis uses to feed on human tissue, have been found in 96% of brains analyzed by Cortexyme and P. gingivalis proper has been found in several brains upon autopsy. Higher rate of these “feeding enzymes’ called gingipains have been higher in those with a greater cognitive decline before their death as well as greater amyloid and tau accumulations.
Cortexyme has developed a molecule with inhibits these gingipains and has shown to effectively halt P. gingivalis infection in mice including stopping amyloid production and reducing the associated brain inflammation.

Connections

                      I can see a connection with the research that they are doing with Koch’s postulates. Not only have they found the pathogen in unhealthy mice, but also upon injecting the pathogen into healthy mice, they receive the same symptoms. I don’t know their exact procedure, however that they are not only exploring what they are finding within the diseased subjects, but duplicating the symptoms in healthy subjects is similar to how they have been identifying pathogens using these postulates.

Critical Analysis

I am very interested in this news story, not only because the community is expanding their thinking on the amyloid and tau protein buildup (previously thought to build up due to cell component aging) being a response to something, rather than an inevitable state of neural tissue. I also like that it goes into light detail on the reasoning behind why they began the studies, what the studies are doing and what the future of the studies are going to be. Also, it is interesting that they have not only made this correlation, but that Cortexyme has already begun developing a vaccine and medications to stop the proliferation of P. gingivalis in the brain (which could also help with gum disease, but I really just love the brains).
As for the article, I think that it is a lot of information for one article but that it is very well put together in a manner that doesn’t overwhelm the reader. There are also links embedded within the article that reference journal articles for further reading, which is beneficial for those who would like a deeper understanding.

Question

The main question that I have is one of correlation vs. causation. There is evidence form the research on healthy mice that the P. gingivalis causes the anomalies within the brain tissue, but they did not find evidence of the bacterium in all cases of Alzheimer’s that they studied. So my question is still the age old question: Is this THE cause of Alzheimer’s disease or is it A cause of Alzheimer’s disease? Does it simply exacerbate the disease or increase the rate at which the disease presents?

 

Samantha Smith

A2 Microbes in the News

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Article and link

“Gene expression study sheds new light on African Salmonella’
Science Daily, January 15, 2019 https://www.sciencedaily.com/releases/2019/01/190115144045.htm

Further Reading: https://www.ncbi.nlm.nih.gov/pubmed/30645593

 

Summary

A variant of Salmonella typhimurium (ST) 313 is responsible for the deaths of approximately 400,000 persons ever year in sub-Saharan Africa. Researchers at the University of Liverpool are attempting to understand how the genome of African S. typhimurium, which enters the bloodstream and spreads through the body, differs from the global strains of S. typhimurium which causes gastroenteritis.

By culturing the different Salmonella strains in different environments they could simulate differences of stages within the human infectious timeline. They then analyzed the transcriptome of these two strains and found a multitude of gene expression variations as well as RNA variations. These coincided with metabolic and plasmid differences within the two strains.

Connection

This correlates with the information that we have learned about variations in culture mediums in class. As well as what we will be going over in lab. The ability to culture this bacterium in different environments allowed for the researchers to study the gene expression at essentially different time frames in the bacterial life cycle. Say, from an environment similar to that outside of the human body, and then an environment within the human body.

Critical Analysis

What I found interesting in this article is that the phenotypic expression of genes within one strain has caused such a different in its ability to act as a pathogen. I also never thought of culturing microbes in different environments to simulate gene expression. I just thought you would culture them in their ideal environment and study them as such. Thinking about it now, it makes a great deal of sense to do this, not only to study the activity of pathogens, but to perhaps study microbes and why they fit into their respective niches.

The forum for this article is a scientific forum, and though it is technical it is written in a way that someone who isn’t specifically a microbiologist (such as myself) can understand what is being studied and the accomplishments that this group of researchers have made.

Question

The question that I have is a technical one. How is it that they were able to find out the gene expression of these bacterium from culture? I know that the genome can be sequenced using various methods, but how would one know or ascertain which portions of that genome are being expressed at any given time.

-Samantha Smith

A3: Epithet Epitaphs

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Coxiella burnetii is a gram-negative rod shaped bacteria first isolated in the 1930s by both Frank MacFarlane Burnet and Herald Rea Cox. Though both Burnet and Cox isolated this bacterium in 1930s they did so independently. While Burnet and his associates were working on the isolation of  the pathogen associated with Query Fever in Australia, Cox was working on the isolation of the pathogen in Nine Mile Valley of Montana. Thus, the bacteria was renamed from Rickettsia burnetii to Coxiella burnetii in 1948 once it was realized that the two research groups were working on the same pathogen (Minnick & Raghaven, 2014)

Given this incidence of naming. There is no Latin Binomial name correlation other than the accreditation of these two researchers with the discovery.

Frank Macfarlane Burnet (1899-1985) was born in Traralgon, Australia. Upon accreditation and finalization of medical school at the University of Melbourne he received his Ph.D. from the University of London. One of his early achievements included developing the technique of culturing viruses in chicken embryos. He also developed the clonal selection theory of antibody formation which laid the foundation for modern immunology. (Britannica) For his work on Immunology and virology he was awarded the Copley Medal in 1959. The following year he was awarded to Sir Frank Macfarlane Burnet and Peter Brian Medawar for their combined discovery of acquired immunological tolerance.

Herald Rea Cox (1907-1986) was born in Terre Haute, Indiana and obtained his doctorate from Johns Hopkins Bloomberg School of Public Health.  (Herald R. Cox, ScD, 2017) He joined the U.S. Public Health Service in 1930 and began studying Mountain Spotted Fever or “Nine Mile Virus’ isolating the Coxiella burnetii in 1938, which allowed his development of vaccines to combat Rocky Mountain Spotted Fever (Q Fever) as well as for several strains of typhus.  In 1942 he moved to New York and became the chairman of the Virus and Rickettsia Research Department where he a worked in conjunction with several other researchers to develop the Polio vaccination (H.R. Cox, 2018)

References

Britannica, E. o. (n.d.). Sir Macfarlane Burnet Australian Physician. Encyclopedia Britannica. Retrieved 20 January, 2019, from https://www.britannica.com/biography/Macfarlane-Burnet

H.R. Cox. (2018). Revolvy. Retrieved from https://www.revolvy.com/page/H.-R.-Cox

Herald R. Cox, ScD. (2017). Johns Hopkins Heroes of Public Health. Retrieved January 20, 2019, from https://www.jhsph.edu/about/history/heroes-of-public-health/herald-cox.html

Minnick, M., & Raghaven, R. (2014, July 21). Genetics of Coxiella burnetii: on the path of specialzation. Future Microbiology, 6(11), 1297-1314. doi:10.2217/fmb.11.116

 

Samantha Smith

A1 Introduction

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Hey Everyone!
My name is Samantha Smith and I am a Biological Sciences Major with a concentration in Physiology and a Minor in Psychology. I am from Louisiana, where the coldest it ever gets is maybe 30*F and most of the year is spent in shorts and flip flops, so the weather adjustment still makes me a little grumpy, though I have been here for slightly over 2 years now.
A few more quick facts: I have a wonderful daughter who thoroughly enjoys collecting various water samples (Puddles, lakes, streams) and trying to find things in her microscope. The only thing she enjoys more is collecting rocks, and one day I will be overrun with vials of water and heaping piles of rocks. I also have three very pleasant dogs which keep up on our toes.

See everyone in class!

Samantha Smith