I am a bug, a proud bacterium who like my other fellow parasites as you may want to call us, make you pretty sick and weak. My full name is Salmonella enterica typhi, a serovar of Salmonella enterica. This means that I belong to the genus Salmonella, a beautiful name which we did not inherit from our fore-fathers but acquired it from Dr Daniel Salmon, who first studied much about us (Chugh et al, 2008). Like my fellow S. enterica serovars; Salmonella Typhimurium and S. Enteriditis, I cause serious diseases in the human intestines. Despite our closely identical features, we are certainly different from each other (Younus, 2014). Personally, I dedicate my energies to causing typhoid fever among humans and am sorry to say that it is so much fun.
As I said, my area of specialisation is nailing humans down with typhoid fever, which affects approximately 17million humans each year. My human hosts that succumb to this disease due to our expansive growth in them total up to 600, 000 in number (Younus, 2014). I am an obligate parasite and just for your information I have no other reservoir apart from humans. While humans know little about the emergence of my infections, they believe I brought about the deaths of famous humans including Rudyard Kipling the British poet, Wilbur Wright who invented the aeroplane and Alexander the Great from the Greek Empire (Chugh et al, 2008). Humans have recorded the earliest epidemic I caused in Jamestown, VA in the 17nth Century where I took about 6,000 humans to their graves through typhoid fever. While the illness I bring about is rare in the USA among other developed countries, it still threatens humans with possible re-emergence.
I was originally isolated by a scientist known as Karl J. Erberth in 1880. I am a multi-organ pathogen and therefore my home can be in the lymphatic tissues of particularly small intestines, the liver, bloodstream, or in the spleen of humans (Garrett, 2016). I am not known to dwell in animals except that I really enjoy operating in developing countries where there are poor sanitary systems; a good environment for me and my family to dwell (Younus, 2014). In these countries, there are inadequate antibiotics against me and therefore humans who travel to Asia, Africa and even Latin America remain at a higher “risk” of having a taste of my effects.
A Microbiological View of Who I am
While I agree that I am very minute to merit being sighted by the naked human eye, I really enjoy bringing them down through spreading and destroying their organs bit by bit. I am a gram-negative and enteric bacillus bacterium belonging to the Enterobacteriaceae family. I am very motile but mainly a facultative anaerobic bacterium that is however susceptible to several antibiotics. Today, more than 107 strains of me have been isolated in the laboratory (Garrett, 2016). Many of my strains already isolated contain metabolic characteristics that vary in nature. They also have different virulence levels, apart from varying multi-drug resistance genes which also enable me to complicate the treatment of typhoid fever in humans especially in those areas where we have managed to make resistance to antibiotics prevalent(Younus, 2014). Apparently, humans are always on track to study us through diagnostic identification and therefore they feed us on MacConkey and EMB agars. This is because they understand that myself including my strains remain strictly a non-lactose fermenting bacteria in nature. I am however identified and distinguished from other Enterobacteriaceae because I never produce gas particularly when being cultured in TSI media (Garrett, 2016). I guess you also don’t like producing gas! Do you?
Typhoid/ Enteric Fever
When I infect an individual, they develop typhoid fever also referred to as enteric fever. Individuals with typhoid fever present with sudden onset of a sustained and/or systemic fever, nausea, lack of appetite, severe headache, constipation including diarrhoea, and spleen enlargement. Further, I also bring about a possible meningitis development, apart from causing general malaise in these humans (Chugh et al, 2008). In cases where we are not effectively destroyed by antibiotics and more so where we individuals are left untreated from typhoid fever, we lead to about 12-30% mortality rates. However, treatment from typhoid fever saves these individuals with a whole 99% survival rate (Younus, 2014). This means that we have been destroyed by antibiotics within their organs.
I have a number of characteristics which make me a real bug or a very effective pathogen if you like it that way. First, I got an endotoxin that is very typical of any given gram-negative micro-organisms. I also have the famous Vi antigen that enables me increase my virulence in human organs. I even produce and excrete invasion protein which allows cells that are non-phagocytic s to take me up like a baby in order for me to live inside them (Mweu & English, 2008). It is apparently so much fun you know. Further, I am very capable of inhibiting the oxidative burst of the human leukocytes, and thus rendering their innate immune response very ineffective. With these characteristics, I float like a butterfly and sting like a bee.
Humans encounter me through the faecal-oral route particularly from individuals who have my colonies to those that are healthy. Patients who practice poor hygiene will most definitely accumulate more of us and therefore acquire a secondary infection. Those who also consume shellfish from water bodies that have our colonies will most likely acquire typhoid fever in the short run (Garrett, 2016). Even so, humans understand that the commonest infection source of infection is drinking water which has been polluted by urine and/or faeces of those individuals infected by our numerous colonies. It is approximated that the inoculum size of our colonies, enough to bring about typhoid fever is100, 000 bacteria (Mweu & English, 2008). This condition (typhoid/enteric fever) is reported by humans to be the commonest reported lab infection.
Our triumphant entry into the bodies of humans is achieved commonly through them ingesting us. Even so, we cannot be transmitted from an infected individual to a healthy one through aerosol means as up to date. Once we are ingested, we multiply in the human small intestine within a period of between 1 and 3 weeks (Guha, 2016). We then gallantly breech the intestinal wall, in order to spread to several other body organs and/or tissues. We are at this stage very effective and the innate host defence system does very little to stop or prevent our destructive effects. This is because we are able to induce the inhibition of the oxidative lysis while at the same time being taken up by cells within which we grow once taken up (Mweu & English, 2008). I have been shown to be transmitted mainly through the faecal-oral means from the asymptomatic individuals. It is also shown that 2-5% of individuals who were previously infected by my colonies remains chronic carriers but yet show no signs of typhoid fever (Garrett, 2016). They however shed us in stronger forms that we are able to infect other humans. The famous Mary Mallon a food handler that led to the infection of about 78 people and death of 5 was a carrier of my colonies (Toichuev, 2011). Such carriers are very dangerous to the public health sector according to human reports as they never show symptoms of our presence, yet they pass our colonies to others. The destruction that I cause to the human organs is however reversible and even limited especially where humans start bombarding me with antibiotics early enough before my colonies multiply (Wang et 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.
The main prevention measure that humans can use to avoid my feasting trend on them is through prevention of faecal contamination of their drinking water and their food supplies (Wang et al, 2014). As they well know that the main source of my colonies is the infected individuals within their population, humans need to control my transmission through proper; hygiene practice, waste management approaches, purification of water, and the effective treatment of the sick(Guha, 2016). The measures I have suggested here to effectively reduce my population are achieved mainly in developed societies leading to the low incidence of typhoid fever. The US for instance, gets about 400 infections each year but almost exclusively in people that have travelled recently to developed countries (Garrett, 2016). I can also be prevented through a vaccine that however remains questionable in effectiveness as I breech its efficacy several times. Further, where humans use large inoculum sizes we obviously overwhelm body immunity already developed against and lead to disease, making them pay for their sins.
In conclusion therefore, the disease I cause has been so significant in history. While I thrive in developing societies, an area that has disasters leading to compromised sanitation is my best dwelling place (Toichuev, 2011). Today humans are in fear of my outbreaks and/or epidemics that could be substantial and therefore I remain a worldwide threat especially due to travelling and no ease of identifying my carriers (Guha, 2016). It is however threatening to me that more development of antibiotic treatments including vaccines could destroy a lot of our colonies and a huge section of our population worldwide. I still start to be counted though, as a gallant bug in the human history. As they write their history, they cannot fail to mention my name.
Chugh, T., Kothari, A. and Pruthi, A. (2008). The Burden of Enteric Fever. The Journal of Infection in Developing Countries, 2(04).
Garrett, D. (2016). The surveillance for enteric fever in Asia project (SEAP): Estimating the community burden of enteric fever. International Journal of Infectious Diseases, 45, p.64.
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. and English, M. (2008). Typhoid fever 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 Effect of Climate Change and Environmental Pollution on Seasonal Fluctuations of Typhoid Fever. Epidemiology, 22, p.S19.
Wain, J. (2008). Why a special issue of JIDC on enteric fever?. The Journal of Infection in Developing Countries, 2(04).
Wang, Y., Huang, K. and Huo, Y. (2014). Proteomic comparison between Salmonella Typhimurium and Salmonella Typhi. Journal of Microbiology, 52(1), pp.71-76.
Younus, M. (2014). Typhoid fever (salmonellosis) as a public health problem by consuming meat and eggs of the carrier birds. Epidemiology: Open Access, s1(01).