Salmonella
Scientific name of the causative organism: Different serovars of Salmonella enterica
I. Classification
Superkingdom: - Bacteria
Kingdom: - Bacteria
Phylum: - Proteobacteria
Order: - Enterobacteriales
Family: - Enterobacteriaceae
Genus: - Salmonella
Species: - S. enterica.
Strain: Salmonella enterica has more than 2500 strains of which Typhi and Paratyphi are the most common.
II. Structure and morphology
If bacterial:
Shape: Salmonella are rod shaped bacteria with diameters ranging from 0.7 to 1.5µm and about 2 to 5µm in length.
Arrangement:
Glycocalyx:
Cell wall: Bacteria of this genus are gram negative.
Cell wall components: S. Typhi has a Polysaccharide capsule Vi on its surface (Fang et al., 2010).
Appendages: Bacteria of the Salmonella genus have plasmid-encoded flagella.
Reproduction: Salmonella like many other bacteria reproduces asexually by binary fission.
Physical requirement for growth:
Temperature range: 400F to 1400F.
Oxygen: Bacteria belonging to this genus are facultative anaerobes.
PH range for growth: 4.1 to 9.2
Disease Dynamics:
Modes of transmission: Direct, indirect, (food, water or other) vector, fomite or other. How is the disease spread and what factors contribute to the spread of the disease in humans or in reservoirs?
Both enteric fever and gastroenteritis are spread indirectly via the consumption of food or water contaminated with Salmonella. However, recent research shows that the disease can also be spread directly from one person to another for some strains of Salmonella. Poor personal and environmental hygiene are some of the factors that contribute positively to the spread of the disease. Lack of clean drinking water is another factor that has been shown to encourage the same. Lack of a system that is able to guarantee the safety of food has similarly been implicated in contributing to the spread of the disease (Simcock, 2004; Fang et al., 2010).
Reservoir: Humans, animals or environment (soil, water, other)
Accurate identification of the reservoirs for Salmonella responsible for human infections is nearly impossible because only a few of the Salmonella serovars are host-restricted or adapted to a specific host. However, both humans and animals act as natural reservoirs of different kinds of Salmonella serovars. Plants like spinach and animal products like eggs, meat also act as reservoirs although the mechanism through which they achieve this is yet to be elucidated upon (Fang et al, 2010; Raffatellu et al., 2008).
How does the organism infect humans and what tissues are targeted?
In both diseases, Salmonella targets the tissues of the intestinal tract although they can seed to other tissues such as the brain, spleen, liver and bones in immunocompromised patients. For enteric infection, Salmonella upon ingestion utilizes a number of mechanisms to invade and change the intracellular environment of host mammalian cells. It employs T3SS encoded by SPI-1 to invade the intestinal epithelium. A group of genes called Salmonella pathogenicity island 2 (SPI-2) encodes type III secretion system which secrete effectors that remodel the microtubule cytoskeleton, induce changes in vesicular transport as well as cause reorganization of the endosomal system. As a result, a Salmonella containing vacuole under the complete control of the pathogen is created which enables the Salmonella enteric serovar Typhi to survive within host cells. For gastritis, the Salmonella serovar responsible uses TSS3 encoded by SPI-1 and SPI-2 to cause an acute intestinal inflammation. Acute inflammation on the other hand provides a new electron acceptor which enables the infective organisms to outcompete the normal gut microflora. Increased colonization of the gut by Salmonella in turn facilitates further transmission of the infective organisms upon fecal shedding (Fang et al., 2010).
What are the symptoms of the disease?
Classic symptoms of an infection by S. typhi or S. paratyphi include high fevers, aneroxia, diarrhea, splenomegaly, abdominal tenderness and signs of anaemia such as fatigue (Simcock, 2004). Patients with gastroenteritis on the other hand present with fever of an acute onset, diarrhea and abdominal cramping (Acheson & Hohmann, 2001).
What is the incubation period, the typical length of illness, recovery time and is there acquired immunity to the infection?
Gastroenteritis has an average incubation period of 12 to 72 hours while the incubation period for typhoid fever is about two to three weeks. Whilst the typical length of illness of gastroenteritis is less than 10 days, symptoms of typhoid fever have a longer duration persisting for up to three weeks. The recovery period for patients with gastroeneteritis is also shorter; the infection clears in a number of days compared to that for enteric fever. Patients who have suffered from bouts of either gastroenteritis or typhoid fever gain acquired immunity against the organisms (Raffatellu et al., 2008).
What treatments and prevention are available?
Third generation cephalosporins and fluoroquinolones are currently the drugs of choice for the treatment of typhoid fever. Use of antibiotic therapy in the management of gastroeneteritis in healthy subjects is however controversial since antibiotics are thought to delay the fecal shedding of the infective organisms and hence elongate the duration of the acute infection. Fluoroquinolones, ampicillin, trimethoprim-sulfamethoxazole and third-generation caphalosporins are however the drugs used to treat severe cases of gastroenteritis (Acheson & Hohmann, 2001). Two types of vaccines that confer protection against typhoid fever are currently available. People travelling to developing nations from the more industrialized nations are advised to be vaccinated against typhoid. Other prevention measures entail provision of clean water and provision of a good sewerage system. Thoroughly cleaning equipment used in the preparation of food products is another prevention method that is used. Last but not least, storing foods at temperatures that discourage the growth of Salmonella is another measure used to prevent Salmonella infections (Fang et al., 2010).
What are the virulence factors? What are the susceptible populations (and why) and where (what areas of the world or what populations) is
the disease found? Is this an opportunistic infection?
The polysaccharide capsule Vi expressed by S. Typhi which inhibits the binding of the O antigen to the O antibody is one of the Salmonella virulence factors. Other virulence factors include flagella, SPI-1 T3SS and SPI-2 T3SS which play a key role in inducing inflammation during the early and late phase of the disease. Gastroenteritis and enteric fever can be opportunistic infections in people who have a weakened immunity for instance, those suffering from Hodgkins disease. People from poor socioeconomic backgrounds are susceptible to the disease by virtue of their living environments since they tend to live in areas with poor sanitation and to lack access to clean water. As such, enteric fever is common in developing nations. People with certain HLA alleles are also thought to be at an increased risk for salmonella infections although the reason behind it is poorly understood. In addition, the very young, the elderly and people who are immunocompromised have a higher than normal risk of getting a Salmonella infection. This is primarily because their immune systems are weak and hence unable to effectively fight off such as infection (Fang et al., 2010).
Epidemiology:
What is the incidence of this disease? How prevalent is it world-wide and in the US? What is the mortality rate? What factors contribute to the distribution of the disease?
The global incidence of enteric fever is estimated at more than 21 million cases annually and it’s mainly prevalent in the developing world especially in Asia and in Africa. The disease is responsible for causing more than 200,000 deaths each year and hence the case fatality rate is estimated to be at 1%. In the US, the incidence of the disease is stands at a moderate figure of 400 cases each year. Factors that contribute to the distribution of the disease include poor sanitation and lack of access to clean water. Meanwhile, the incidence of gastroenteritis in the US is estimated at 14 to 15 per every 100 000 population with a case fatality of less than 1%. The global incidence of Salmonella gastroenteritis is approximated to be 98.4 million cases per year of which 155 000 deaths occur annually. Gaps in the systems meant to ensure food safety, poor personal and environmental hygiene, and limited knowledge of the ecological determinants of food contamination by Salmonella are some of the factors that have positively contribute to the spread of Salmonella gastroenteritis (Fang et al., 2010).
References
Acheson, D., & Hohmann, E.L. (2001).Nontyphoidal salmonellosis. Clinical Infectious Diseases,
32(2), 263-269. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed
Fang, F.C., Andrews-Polymenis, H.L., Baumler, A.J., McCormick, B.A. (2010). Taming the
elephant: Salmonella biology, pathogenesis and prevention. Infect Immun., 78(6), 2356–
2369. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed
Raffatellu, M., Wilson, R.P., Winter, S.E., & Baumler, A.J. (2008). Clinical pathogenesis of
typhoid fever. J Infect Developing Countries, 2(4), 260-266. Retrieved from
http://www.ncbi.nlm.nih.gov/pubmed
Simcock, D. (2004). Gastroenteritis, fever and myoglobinuric renal failure. J R Soc Med., 97(4),
185–186.Retrieved from http://www.ncbi.nlm.nih.gov/pubmed
