Serratia Marcescens

In this lab, the organism that we have been working with is the bacterium, Serratia marcescens. S. marcescens is a member of the Enterobacteriaceae family, and tends to grow in damp environments. S. marcescens is an ideal bacterium to work with in the lab because it reproduces quicker than other bacterium. This bacterium produces a special pigment called prodigiosin, which is red in color. The prodigiosin pigment is intensified when S. marcescens is grown at higher densities. During our experiment, temperature, pH, salinity concentration and oxygen requirements were tested on S. marcescens to measure their optimal growth and prodigiosin production.

Abstract-The gram-negative bacteria Serratia marcescens has gained attention in recent years for its tendency to cause nosocomial infections in humans, as well as its development of antibiotic resistance. Antibiotic resistance in a bacterium that is harmful to humans can be concerning as it can result in infections that are difficult to treat. In order to find out more about the growing antibiotic resistance of S. marcescens, this experiment used the disc diffusion method to test the susceptibility of S. marcescens to two varieties of antibiotics that were known to have success against some gram-negative bacterium: streptomycin and ampicillin. These antibiotics were, respectively, an aminoglycoside and a beta-lactam. The experiment tested which of the two that S. marcescens had developed more of a resistance to. The zones of inhibition of the discs were significantly larger for discs treated with streptomycin compared to discs treated with ampicillin. This led to the conclusion that S. marcescens is less resistant to streptomycin than to ampicillin.

Most species of Serratia are of human (fecal) origin. Usually S. marcescens is found in as a nosocomial infection in the urinary and respiratory tract, in cystic fibrosis, and in burns (Deguzman, 2012).

The genus Serratia a member of the Enterobacteriaceae bacteria. It was once in soil, insects and plants and became more frequent in the nosocomial infections. The S. marcescens strains are now a serious threat in surgical and intensive care units. The Serratia infection

Serratia Marcescens is a rod (bacillus) shaped bacteria known best for its red coloration. It has a single arrangement and is Gram negative. It grows at room temperature and can be found in soil, water, animals and on plants, but it is especially common in damp areas such as bathrooms or kitchens. Like all bacteria, it reproduces by binary fission. Serratia Marcescens mainly causes urinary and respiratory tract infections but can also cause pneumonia, bloodstream infections, wound infections, and meningitis along with a variety of other infections. It can be difficult to treat S. Marcescens as it is resistant to various antibiotics. In this experiment we tested the effects of antiseptics on the zone of inhibition on serratia marcescens.

Prediction: If UV light mutates the DNA of Serratia Marcescens then the red pigment colonies of the bacteria will no longer be produced.

First, of the other antibiotics within the rationale, Chloramphenicol was able to create the largest zone of inhibition, with the largest radius of the other two antibiotics, and was able to fully inhibit the growth of Kocuria rosea, without allowing any other bacterial cells to survive within the zone on inhibition. Second, the structure of Chloramphenicol allows it to effectively inhibit the growth of bacteria. Chloramphenicol is an antibiotic with an extremely lipid-soluble structure that allows it to bind to the 70S ribosomes of prokaryotes and inhibit the creation of proteins, or protein synthesis, within that prokaryote. This is able to be accomplished by the antibiotic because it is able to prevent the peptidyl transferase activity within the ribosome, and this causes the inhibition of bacterial growth because Peptidyl transferase is vital in the translation process of protein synthesis, a process in which peptide bond are formed between amino acids through the use of tRNA. Therefore, because all bacteria are unicellular organisms, the structure of Chloramphenicol allows it to be effective against almost all bacteria, thus proving itself to be the best antibiotic to combat this strand of bacteria. And finally, resistance towards Chloramphenicol is very minimal within bacterial strands. High-level resistance towards Chloramphenicol can only be created through a mutation in the 50S ribosomal subunit of a bacterial cell, which creates a gene that codes for an enzyme, known as Chloramphenicol Acetyltransferase, which has the properties to inactivate Chloramphenicol. However, this resistance mutation within the 50S ribosome is extremely rare and resistance towards Chloramphenicol can be reduced if this antibiotic is used only when necessary, on patients who absolutely need the antibiotic in order to

I discovered that my unknown organism was Serratia marcescens. This organism is gram negative and bacillus shaped. It is a member of the Enertobacteriae family. This organism appears a red blood like color when it grows on media. It is anaerobic, but can also survive under aerobic conditions. There are some strains of Serratia marcescens that are motile and have flagellum. It is able to produce the enzymes chitinase, lipase, protease, nuclease, and serrawttin. It is a non-endospore forming bacteria, chromogenic, and does not ferment lactose. (Falkiner, 1997)

Bacteria grows by binary fission. The aim of this experiment is to follow the growth of Serratia marcescens in nutrient broth at 37oCby recording the changes in turbidity (cloudiness) by measuring the absorbance of visible light (600 nm) and also to prove that there is an increase in the cell number and not just in mass during the growth. In the experiment we measure the full growth curve of Serratia marcescens by measuring the absorbance at 600nm at every 10 mins. I also determined the viable count at the start and the end of the exponential phase of growth. Using the growth curve I calculated the growth curve and it was 1.2. Using this I found the doubling time which was 34s.

If I received the NH Grant, I would use the money to further my knowledge and study of Neagleria fowleri. Neagleria fowleri is an amoebaflagellate and amoebas are microscopic single-celled organism. N.fowleri was first discovered in 1965 in Australia by scientist M. Fowler and R.F. Carter, but N.fowleri is most commonly found in the United States. When they found N.fowleri, it was a huge discovery. This amoeba showed scientist that an amoeba can function and live in a human host but also in nature. N.fowleri is found mainly in warm bodies of water. There has been 150 documented cases in the United States since 1965-2014. N.fowleri is also extremely deadly; the fatality rate is 99%. The amoeba itself isn’t deadly, the disease that it causes is what kills people. That disease is called Primary amebic meningoencephalitis or PAM. Neagleria fowleri is so rare that many people have never even heard of this amoeba, so with this grant I want to make Neagleria fowleri more known to the public so people know how to prevent this deadly amoeba.

Two years ago I went to an exhibition in Milan titled: “Artemisia: storia di una passione” (“Artemisia: history of a passion”). The exhibition was sponsored by the Assessorato alla Cultura of the Comune of Milano and curated by Roberto Contini and Francesco Solinas, with the scenographic and theatrical work of Emma Dante.

Working with serratia marcescens and prodigiosin can be such a normal thing and maybe even routine for scientists or their students but not all care to know the background of its origins and where the pigment comes from. Its obvious that we all notice pigment while experimenting with Serratia marcescens  and its best known for the red coloration itself that is produced through strains in the bacteria all connected to a term, Prodigiosin. Prodigiosin is essentially not manufactured at 37°C, but preferably at temperatures below 30°C. The coloration will not be seen in the strains if the conditions don’t connect. All of the environmental conditions in this experiment were tested at 0, 30, 60, 90, 120, 150, and 180 minutes, wavelengths

These mutations, no matter what process that has led to their occurrence, block the action of antibiotics by interfering with their mechanism of action (1). Currently, antibiotics attack bacteria through one of two mechanisms. In both mechanisms the antibiotic enters the microbe and interferes with production of the components needed to form new bacterial cells. Some antibiotics act on the cell membrane, causing increased permeability and leakage of cell contents. Other antibiotics interfere with protein synthesis in cells. They block one or more of the steps involved in the transformation of nucleic acids into proteins.

Why exactly is Artemisia Gentileschi considered an early feminist? Doing a brief search and looking into her artwork, even for a brief amount of time and you quickly see why she was considered so. Her gender as well as the things she went through and experienced in her life heavily influenced Artemisia Gentileschi’s artwork. Some of the more famous and controversial paintings focus on females as being the main protagonist. There is plenty of controversy surrounding the paintings as well, since her father Orazio Gentileschi a painter in his own right trained her. Some of her early paintings are questioned and he is given credit for them.

There are numerous way a bacteria can gain resistance to an antimicrobial agent as such through spontaneous mutations specifically by the alteration of the ribosomal target sites. Generally, tetracycline resistance may be mediated by various mechanisms, however, the most common method are the ribosomal protection mechanism. Tetracycline resistance results when this antimicrobial agent failed to bind to its target sites or sites on the ribosome and thus disrupts its ability to halt protein synthesis and cell growth in the bacteria. According to Bennett, Dolin and Blaser (2014), tetracycline resistance has been widely observed in Helicobacter pylori, where this organism possess a mutation in its 16S rRNA that restricts the tetracycline binding