This is the creative essay.
* This assignment will be done individually by students. You will need to tell a non-technical “story” from a microbe’s point of view (i.e.
You will be the microbe, and you will tell your story in a scientifically sound language that a 1st-year university science student can understand.
* Students will be required to select a microbe (either a virus, bacteria or parasite), and then develop key ideas that will serve as the basis for their essay (decribing the pathogenesis of the microbe they choose).
I am a bug. A proud bacterium. You will be pretty weak and sick if you are like me, my fellow parasites.
This means I am a member of the genus Salmonella. It is a beautiful name that we didn’t inherit from our forefathers, but Dr Daniel Salmon gave it to us. (Chugh and al., 2008).
As my fellow S. enterica serovars, Salmonella Typhimurium & S. Enteriditis respectively, I can cause serious intestinal diseases.
Although we share many similarities, our differences are clear (Younus 2014).
Typhoid fever is something I enjoy doing and it’s a lot of fun.
My area of expertise is Typhoid fever. This disease affects around 17 million people each year.
Our rapid growth has caused this disease in 600,000 of my human hosts (Younus 2014).
I am an obligate parasite. You should know that I have no other source of food than humans.
Although humans don’t know much about my infection, they believe that I caused the deaths of many famous people, including Rudyard Kipling, a British poet, and Wilbur Wright, who invented the plane, and Alexander the Great, from the Greek Empire (Chugh, et al., 2008).
Humans can remember the first epidemic I created in Jamestown, VA in 17th century. I killed approximately 6,000 people with typhoid fever.
Although the disease I cause is uncommon in the USA and other developed countries it still poses a threat to humans.
Karl J. Erberth, an 1880s scientist who isolated me, was the original one.
My home is in the lymphatic tissues of the liver, small intestines, bloodstream and spleen of humans. I am a multi-organ pathogen (Garrett 2016).
I have never been known to live in animals, but I do enjoy working in countries with poor sanitation systems. This is a great environment for me and my family (Younus 2014).
These countries lack adequate antibiotics and I am at greater risk of getting my effects. Humans who travel to Asia, Africa, and Latin America are therefore at higher risk.
A microbiological view of who I am
Although I do agree that I am too small to be able to see the naked eye, I enjoy helping them by spreading their organs and breaking them down.
I am a Enterobacteriaceae gram-negative, enteric bacillus bacteria bacterium.
Although I’m very mobile, I am primarily a facultative anaerobic bacteria that is susceptible to many antibiotics.
More than 107 strains have been identified in the laboratory today (Garrett 2016,).
My strains have metabolic characteristics that are different from their natural counterparts.
They also differ in virulence, as well as varying multi-drug resistant genes, which allows me to complicate treatment of Typhoid fever in humans, especially in areas where antibiotic resistance is prevalent (Younus 2014).
Humans are always keen to learn more about us, so they give us MacConkey and EMB agars.
They know that I, and my strains, are strictly non-lactose fermentation bacteria.
However, I can be identified and distinguished from other Enterobacteriaceae due to the fact that I don’t produce gas when cultured in TSI media (Garrett 2016,).
You don’t like making gas, I suppose!
Typhoid/ Enteric Fever
Typhoid fever is also known as enteric fever.
Typhoid fever is characterized by a sudden onset of systemic and/or sustained fever, nausea, vomiting, severe headaches, constipation, diarrhoea and enlarged spleen.
In addition to causing general malaise, I can also cause meningitis and possibly even cause it.
We can lead to a 12-30% mortality rate in cases where we aren’t effectively killed by antibiotics, and even more when we leave untreated from Typhoid fever.
Typhoid fever treatment saves these people with a 99% survival rate (Younus 2014).
We have been rendered unintelligible by antibiotics in our organs.
If you want to call me a bug, or an effective pathogen, I have many characteristics.
First, I have an endotoxin which is typical of all gram-negative microorganisms.
The Vi antigen is also present, which allows me to increase my virulence in the human organs.
Invasion protein is a protein I produce and excrete that allows non-phagocytic cells to raise me like a baby to allow me to live within them. (Mweu, English, 2008).
You’ll find it so much fun.
Additionally, I can inhibit the oxidative burst in human leukocytes and render their innate immune system very ineffective.
These characteristics allow me to float like a butterfly while stinging like a bee.
I am commonly encountered by humans through the faecal/oral route, especially from those who have my colonies to those who are healthy.
Poor hygiene can lead to more infections and more patients will end up with us.
Typhoid fever is most likely to be contracted by those who eat shellfish from bodies with our colonies (Garrett 2016).
Humans know that drinking water polluted with urine and/or faeces from infected individuals is the most common source of infection.
The inoculum of our colonies is sufficient to cause typhoid fever (Mweu and English, 2008).
Typhoid/enteric fever is the most common reported laboratory infection.
Commonly, our triumphant entry into the bodies and minds of other people is accomplished by them ingestion.
However, we are not able to be transmitted via aerosols from infected individuals to healthy ones.
We multiply within the small intestine of humans after we are inhaled (Guha, 2016).
The intestinal wall is then broken and spreads to other organs and tissues.
At this point, we are very efficient and the innate host defense system is unable to stop our destructive effects.
Because we can induce inhibition of oxidative lysis and be taken up by cells, we then grow (Mweu English, 2008).
My transmission is primarily through the faecal and oral routes from the asymptomatic.
Garrett (2016) also shows that about 2-5% of those who have been infected with my colonies are chronic carriers, but show no symptoms of typhoid.
However, they shed us in stronger forms so that we can infect other people.
Mary Mallon, a famous food handler who caused the infectiveness of around 78 people and the death of five others, was a carrier for my colonies (Toichuev 2011, Toichuev).
Human reports show that such carriers pose a danger to public health because they don’t display symptoms but can pass my colonies on to others.
However, the damage I do to human organs can be reversed and even limited if humans begin to bombard me with antibiotics before my colonies multiply (Wang and colleagues, 2014).
To avoid me feasting on them, humans must prevent faecal contamination in their drinking water.
They know full well that my colony is caused by infected people within their own population. Therefore, they need to prevent my spread through hygiene, waste management, water purification, and treatment of the sick (Guha, 2016).
These measures are mostly effective in reducing my population, and have a low incidence of typhoid.
For example, the US gets approximately 400 infections per year, but this is almost exclusively among people who have recently traveled to developed countries (Garrett 2016,).
A vaccine can be used to prevent me from getting infected. However, its effectiveness is still questionable as I have breeched it several times.
Furthermore, large doses of vaccines can lead to overuse and disease.
The history of the disease that I caused is therefore so important.
Although I thrive in developing countries, my ideal home is an area with poor sanitation and disasters.
People are afraid of me spreading epidemics or other diseases that could be severe. I am a global threat because of the fact that I travel and can’t be identified easily.
However, it is threatening that we may lose a lot of our colonies as well as a large portion of our global population if more antibiotic treatments are developed.
I am still counted, however, as a gallant insect in human history.
They cannot forget to mention me as they write their history.
Chugh, T., Kothari A. and Pruthi A.
The Burden of Enteric Fibro.
The Journal of Infection in Developing Country, 2(04).
The surveillance for enteric disease in Asia (SEAP),: Estimating the community burden.
International Journal of Infectious Diseases 45, p. 64.
Journal of Medical Science and Clinical Research, 04 (12), pp.14855 -14856.
Mweu E. and English M. (2008).
Typhoid fever among children in Africa.
Tropical Medicine & International Health 13(4), pp.532-540.
Journal of Clinical and Diagnostic Research.
The Influence of Climate Change and Environmental Pollution On Seasonal Fluctuations Of Typhoid Fever.
Why is there an issue of JIDC devoted to enteric fever?
The Journal of Infection in Developing Country, 2(04).
Wang, Y. Huang, K. and Huo. Y.
Comparison of proteomic data between Salmonella Typhimurium (Salmonella Typhi)
Journal of Microbiology 52(1), pp.71–76.
Consuming meat and eggs from the carriers of Typhoid fever (salmonellosis), is a public health concern.