HBM2105 Medical Microbiology And Immunity


Question:


The creative essay will be as follows:

* This assignment is for students only. Each student will write a story, non-technical, from the point of an individual microbe.

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You will play the role of the microbe to tell your story, using a language that is simple and scientifically accurate.

* Students will need a choice of a microbe (a bacteria virus, parasite or virus) and will need to develop the key ideas. This will form the basis for the essay that describes the pathogenesis, infection, and consequences of their chosen microbe.

Answer to Question: HBM2105 Medical Microbiology And Immunity

Introduction

I am a bug. My full name is Salmonella enterica typhi, a serovar of Salmonella enterica.

This means that my genus is Salmonella. A beautiful name we did not inherit from our ancestors, but were given it by Dr Daniel Salmon who studied us extensively (Chugh et. al., 2008).

Like my fellow S. enterica serovars, Salmonella Typhimurium (S. Enteriditis), I can cause serious diseases to the human intestines.

Despite having similar features, we are quite different from one another (Younus, 2014.

I am a typhoid fever activist and find it so much fun.

As I stated, my area is Typhoid-Fever. It affects about 17 million people every year.

Our exponential growth in them has led to 600,000.

I am an obligatory parasite.

Humans do not know the exact cause of my infections. They believe I was responsible for the deaths Rudyard Kipling, the British poet, Wilbur W. Wright, the inventor of the airplane, and Alexander the Great (Chugh et. al. 2008).

Humans are able to trace the origin of the first epidemic I caused in Jamestown (VA) in the 17th Century. There, I drove 6,000 people to their graves with Typhoid fever.

Although it is rare in the USA, and other developed countries, it can still pose a danger to human health.

History

Karl J. Erberth (1880) was the scientist who first isolated me.

I’m a multiorgan pathogen. Therefore, my home can be in lymphatic tissues in the liver, bloodstream, and small intestines. (Garrett (2016)

I’m not known to reside in animals. However, I do really enjoy operating in developing nations with poor sanitary systems. This is a great environment for me and my families to live in (Younus – 2014).

Because of the lack of antibiotics, I’m not protected in these countries. Therefore, people who travel from Latin America, Asia, Africa, or Latin America to experience my effects are at greater “risk.”

A Microbiological Perspective of Who I am

While I acknowledge that I am too tiny to be seen by the naked eyes, I find it very enjoyable spreading disease through their organs.

I am a Enterobacteriaceae-family gram negative and enteric bacteria bacterium.

I am quite mobile, but mainly a facultative and anaerobic organism that is sensitive to antibiotics.

Over 107 strains of me were isolated in the lab (Garrett (2016).

Many of my strains are unique in their metabolic characteristics.

They also possess different virulence levels. This allows me to complicate the treatment typhoid-related diseases in humans, particularly in areas that have made antibiotic resistance more prevalent (Younus (2014)).

Humans have a tendency to follow us around and study us via diagnostic identification. They therefore feed us MacConkey agars and EMB broths.

This is because they realize that I and all my strains are non-lactose-fermenting bacteria.

I am nevertheless distinguished from other Enterobacteriaceae, as I don’t produce any gas in culture, particularly when using TSI media. (Garrett 2016).

It’s possible that you don’t like gas production! Do you?

Typhoid/ Enteric Fever

Typhoid fever, also known as enteric or chronic fever, is a condition that I can infect someone.

Typhoid fever can cause a sudden onset, sustained, or systemic fever, nausea and vomiting, severe headaches, constipation and diarrhoea, as well as a swollen spleen.

A possible development of meningitis, as well as general malaise, can be caused by me (Chugh et. al., 2008).

There are 12-30% deaths in cases when we are not treated for typhoid fever and are not effectively eradicated by antibiotics.

The good news is that typhoid flu treatment can save these individuals with a 100% survival rate (Younus, 2014).

This means that our organs are destroyed by antibiotics.

Virulence factors

My characteristics make me an effective pathogen or bug.

First, I was able to get an endotoxin very similar to any given gram negative micro-organism.

I also have the Vi antigen which allows me increase my virulence for human organs.

I even produce and exude invasion protein, which allows cells that have non-phagocytic s for me to be raised like a baby inside their bodies (Mweu&English, 2008).

It is so much fun.

I’m also capable of blocking the oxidative surge of human leukocytes, rendering their natural immune response ineffective.

These attributes allow me to fly like a butterfly, and sting like bees.Epidemiology

People come into contact with me via the faecal and oral route, particularly from people who have my colonies.

Patients who don’t practice good hygiene will more easily accumulate us and thus contract a secondary infection.

In the short-term, those who consume shellfish from waters that contain our colonies will be more susceptible to typhoid (Garrett (2016)

However, it is well-known that water contaminated with our colonies can lead to infection.

According to Mweu & Engle, 2008, the inoculum required for typhoid is 100, 000 bacteria.

The most common lab infection is typhoid/enteric.

Commonly, our triumphant entry into the body of humans occurs through them ingesting.

Although we can be transmitted by aerosol means from an infected person to a healthy individual, it is not possible to transmit the virus to another person.

Guha, 2016, states that once we are ingested we can multiply in the human small intestinale within 1 to 3 weeks.

Our gallantry then allows us to break through the intestinal walls and spread to various other body organs/tissues.

This stage is very powerful and the innate defense system of our host does not do much to stop or prevent us from causing more harm.

This is because we can induce the inhibition of oxidative metabolism while being taken up into cells that we grow once we have been taken up (Mweu, English, 2008).

It was shown that I transmit mainly by the faecal-oral routes of the asymptomatic.

Garrett (2016) shows that 2-5% of my colonies-infected individuals are still chronic carriers of the disease, yet they show no signs of typhoid.

They shed us in stronger, more susceptible forms, so we can infect others.

Mary Mallon, a food worker who was responsible for the infecting 78 people and causing the deaths of 5 others, was also a carrier of my colony (Toichuev 2011).

Human reports indicate that these carriers are extremely dangerous to the public sector’s health as they transmit our colonies to others, despite not showing any symptoms.

However, I can cause irreversible damage to human organs, especially if my colonies multiply before they are too late (Wang und al., 2014). As a result, there is below 1% mortality rate among individuals treated of the disease and caused by my antibiotic-susceptible strain and therefore makes both prognosis and outcome for patients positive.Prevention:

Humans can prevent me from feasting on their bodies by avoiding faecal contamination.

Because they know that my colonies are mainly caused by the infected individuals in their population, people need to manage my transmission using proper hygiene, waste management methods, purification of water and effective treatment for the sick (Guha 2016).

To reduce my population, the measures I suggest here are mainly applicable to developed countries. This results in low rates of typhoid.

For instance, the US is home to approximately 400 cases of typhoid fever each year. This happens almost exclusively for people who have visited developed countries in recent years (Garrett (2016)).

I can also be protected by a vaccine. But, I have repeatedly abused its efficacy.

Additionally, large inoculum amounts can cause immune system over-reactions and result in disease.

In conclusion, the history of the disease I have caused is so remarkable.

Although I thrive in the developing world, I find my home in an area where there are disasters and poor sanitation (Toichuev (2011)).

Today’s humans fear me and my potential epidemics. This is due to the fact that I can travel and it is difficult to identify my carriers. Guha, 2016.

My concern is that the development of more antibiotic treatments, including vaccines may lead to the destruction of many of our colonies and a substantial portion of our population.

I am still considered to be a gallant bug in human history.

They can’t forget to mention my name as they write their histories.

References

Chugh T.; Kothari A.; Pruthi A. (2008).

The Burden and Risk of Enteric Fever.

The Journal of Infection in the Developing Countries, 2(4).Garrett, D. (2016).

The surveillance for Enteric Fever in Asia Project (SEAP): Estimating enteric fever’s community burden.

International Journal of Infectious Diseases. 45.Guha, D. (2016). Neonatal Sepsis Due to Salmonella Typhi – A Case Report.

Journal of Medical Science And clinical Research. 04/12. pp.14855–14856.

Mweu E. & English M. (2008).

Typhoid fever is a common disease in children in Africa.

Tropical Medicine & International Health. 13(4). pp.532-540.Singhal, V. (2012). Neonatal Salmonella Typhi Meningitis: A Rare Entity.

Journal of Clinical and Diagnostic Research.Toichuev, R. (2011).

The Effects of Climate Change on Typhoid Fever Seasonal Fluctuations. Epidemiology, 22, p.S19.Wain, J. (2008).

Why is JIDC publishing an exclusive issue on enteric fièvre?

The Journal of Infection in Development Countries, 2(4).

Wang, Y. Huang K., Huo, Y. (2014).

Comparison of proteomic results between Salmonella Typhimurium, and Salmonella Typhi.

Journal of Microbiology. 52(1). pp.71–76.Younus, M. (2014).

Typhoid fever, also known as salmonellosis, is a public-health problem. It can be caused by eating meat or eggs from the carrier birds. Epidemiology: Open Access, s1(01).


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