Response of Staphylococcus aureus to acetylsalicylate challenge while in the presence of Notatum Penicillium. (this title does not make sense, what is an acetylsalicylate challenge?)
Sarai Finks and Kazuhiro Sabet
Biology 3B, Department of Biology, SaddlebackCollege, Mission Viejo, California(NO)
Bacterial resistance to antimicrobial agents is emerging in a wide variety of pathways taken by pathogens. The ability of S. (italicize) aureus to grow in an acetylsalicylate challenge was tested in the presence of N. (italicize) penicillium. After a 72-hour incubation period the mean diameter of the zone of inhibition around the sterilized chads(what’s a chad? Please define) under non-acetylsalicylic environment was 0.0 ± 0.0cm (± SEM), and the mean diameter around chads under an acetylsalicylic environment was 0.0 ± 0.0cm (± SEM).The mean diameter around the 10g of N. penicilliumunder a non-acetylsalicylic environment was 5.3 ± 0.4cm (± SEM), and the mean diameter around N. penicillium under an acetylsalicylic environment was 8.3 ± 0.6cm (± SEM). There is a significant difference between the four groups (p =, ANOVA). There was a significant difference in the mean diameter around the10g of N. penicillium under an acetylsalicylic and non-acetylsalicylic environment was 5.5%. The mean diameter around the sterilized chads in S. aureus under an acetylsalicylic environment, and the mean diameter around the 10g of N. penicillium in S. (italicize)aureus under an acetylsalicylic environment was 14.2%. This shows a greater inhibition of S. (italicize)aureus in the presence of a 30mM concentration with N. penicillium than with only the affect of N. penicillium on S. (italicize)aureus alone.
Are you sure it isn’t supposed to be Penecillium notatum?
This is way too specific for an abstract. Don’t turn this into the results section.
Why is this giant gap here?
Introduction
S. aureus has the ability to grow in high-salt low moisture environments as well as resist multiple antibiotics in the presence of acetylsalicylate (aspirin) (Riordan, et al., 2006). S. aureus contains a strain that is methicillin-resistant,^.(Capitalize the m) methicillin is in a group of antibiotics called beta-lactams (Lewis et al., 1990) and is a source for many enteric diseases.Investigators were interested in the antibacterial properties that many fungi contain and the properties that bacteria display in response to a threat. Penicillin^, for example^, is an endotoxin excreted from the Penecillium fungi and has beneficial healing properties in that it was first synthesized for use as an antibiotic (Arriero^, 2002). The objective of this experiment was to observe the ability of Notatum Penecilliumto withstand Staphylococcus aureus in the presence of acetylsalicylate (Riordan et al., 2006). Conflicting research exists as to whether acetylsalicylate inhibits or promotes bacterial growth in the presence of an antimicrobial (Arriero^,2002, Lewis 2006). Acetylsalicylate is classified as a nonsteroidal anti^-inflammatory drug (Shiff et al.,1995). It is widely consumed for a variety of ailments ranging from pain to fever. It is also utilized as a means of preventative health measures against cancer and heart disease (Shiff et al., 1995). In this experiment^, acetylsalicylate was a successful growth inhibitor of S. aureus in the presence of N.(italicize)Penecillium, this observation may contribute to a better understanding of the properties and mechanisms of fungi in response to a bacterial threat. It is important to have a deeper understanding of how bacteria can adapt to overcome changes to their environment. Understanding how bacteria adapt and evolve to survive despite the best efforts of the present day antibacterial practices can possible aid in helping to prevent or treat infection (Tenover, 2001).
Materials and Methods
The bacteria S. (italicize)aureus and fungus N.Penicillium were cultured over a 48-hour period. This was to ensure that the appropriate amounts of the organisms were available for plating on 27 plates. A nutrient agar was made by placing 27.6 g of nutrient starter in 1200 ml of water and carefully bringing the solution to a boil. Once the solution was autoclaved at 200º F for 30 minutes the solution was allowed to cool slightly and then poured over 27 sterile plates. The plates were allowed to cool and the cultures of S. areus (250 L) and N. Penicillium (10g) were placed on the plates. The acetylsalicylate solution was made by dissolving 0.324 g of solid acetylsalicylic acid in 60.0 ml of DI water yielding a concentration of 30mM. Ten plates consisted of the S. aureus(250 L), N. Penecillium, and acetylsalicylic acid (250 l). Ten additional plates consisted of S.(italicize)aureus and N.penecilliumin the same concentrations as mentioned above. Seven plates where served as the control. Sterilized chads were placed in DI water and also in the acetylsalicylate solution and placed on opposite ends of the same plate. This was done to observe the affect acetylsalicylate would have on bacterial growth. The plates were all placed in an incubator for 72-hours at 37º C. All temperatures and outside factors were held constant and data was then collected by measuring the halos or zone of inhibition (where bacteria did not grow) around N. penecillium and the chads.
Results:
Figure 1. The bar graph showing mean diameter of the zone of inhibition ± SEM around the sterilized chads and 10 g of N. penicilliumunder an acetylsalicylic and non-acetylsalicylic environment. The figure represents the bacteria, S. (italicize)aureus and the fungi, N. penicillium.
Your error bars are not properly formatted.
The measurements were taken after a 72-hour incubation period. The mean diameter of the zone of inhibition around the sterilized chads under non-acetylsalicylic environment was 0.0 ± 0.0cm (± SEM), and the mean diameter around chads under an acetylsalicylic environment was 0.0 ± 0.0cm (± SEM). The mean diameter around the 10g of N. penicilliumunder a non-acetylsalicylic environment was 5.3 ± 0.4cm (± SEM), and the mean diameter around N. penicillium under an acetylsalicylic environment was 8.3 ± 0.6cm (± SEM). There is a significant difference between the four groups (p =, ANOVA).The Bonferroni correction showed no significant difference between the groups S. aureus in a non-acetylsalicylic environment and S. aureus in an acetylsalicylic environment was 0.0%. There was a significant difference in the mean diameter around the10g of N. penicillium under an acetylsalicylic and non-acetylsalicylic environment was 5.5%. The mean diameter around the sterilized chads in S. aureus under an acetylsalicylic environment, and the mean diameter around the 10g of N. penicillium in S. aureusunder an acetylsalicylic environment was 14.2%.
Discussion:
Based on the results it is thought that there may be some reaction taking place between N. penicillium and the acetylsalicylate that caused a greater inhibition of bacterial growth of S. aureus since there is a difference, although the mechanism is not fully understood . This could be attributed to the specific proteins found with in the cell wall of N. Penecillium and related to the endotoxin that is released from the N. penecillium that gives it its antimicrobial traits. A reaction between the penicillin endotoxin and the acetylsalicylate could produce a greater toxic environment and thereby create a more unfavorable environment for S. aureus to thrive than if just the penicillin were present. This is noted in the difference in the mean zone of inhibition for the bacterial growth and which was 5.3 ± 0.4cm (± SEM) for the group with out the acetylsalicylate challenge and 8.3 ± 0.6cm (± SEM) for the group with the acetylsalicylate challenge. An ANOVA, p =, was then run for all the groups and showed a F-value equal to 100.5 showing a significant difference in the groups. The groups were then compared to each other by running a Bonferroni correction this revealed that there was a significant difference in the zones of inhibition between each group. The group containing S. aureus and N. penicilliumand acetylsalicylate were significantly different than the group containing just the bacteria and the fungi and the group containing only the bacteria and the acetylsalicylate by 5.5% and 14.2% respectfully. Some sources for error may have arose and lead to error in measurements. These sources could be attributed to incorrect plating of the bacteria and the fungi and aspirin. Cross contamination also played a minor role as some of the data had to be negated to over growth of fungus on the bacterial control. The control was very important since we were testing aspirins combined effect with penicillin to inhibit bacterial growth. The control was initially done but only qualitative observations could be made from it since sterilized chads had not been added. A second round of plates containing the bacteria and sterilized chads that had been treated with DI water and with a 30 mM solution of acetylsalicylate was used to quantitatively collect data. The same environment was created for the control and observations and data collected.
References
- A. Claudina, Bachert C, Cauwengberge P, Gevaert P, Holtappels G, Kowalski L. M.,
Kuna Piotr, Novo P, Ptasinka A, Johannson S,. Aspirin Sensitivity and IgE
Antibodies to Staphylococcus aureus Enterotoxins in Nasal Polyposis: Studies on the
Relationship. Int Arch Allergy Immunol 2004;133:255-260.
2. A. P. Sampsonw,C. H. Suh, D. H. Nahm, H. J. Kimz, H. S. Park, S. H. Yoon,Y. J.
Suh. Specific immunoglobulin E for staphylococcal enterotoxins in nasal polyps from
patients with aspirin-intolerant asthma. Clin Exp Allergy 2004; 34:1270–1275.
3. Arriero M. Maria, et al.Aspirin prevents Escherichia coli lipopolysaccarides
and Staphylococcus aureus induced down regulation of endothelial nitric oxide
synthase expression in Guinea pig pericardial tissue. Journal of the American Heart
Association.Circulation Research. 2002;90:719.
4. B Rigas, L L Tsai, L Qiao, S J Shiff. Sulindac sulfide, an aspirin-like compound,
inhibits proliferation, causes cell cycle quiescence, and induces apoptosis in HT-29
colon adenocarcinoma cells. Laboratory of Human Behavior and Metabolism, New
York, New York10021.
5. Bang J, Cho J,Choe K, Kim H,Kim J,Kim S, Oh M, Park Beom W.Effect of
salicylic acid on invasion of human vascular endothelial cells by Staphylococcus
aureus. 2006.00170.
6. Bayer S. Arnold, Filler G. Scott, Kupferwasser Leon Iri,Nast Cynthia C, Shapiro Shelley M, Sullam M Paul,Yeaman R Michael. Acetylsalicylic Acid Reduces Vegetation Bacterial Density, Hematogenous Bacterial Dissemination, and Frequency of Embolic Events in Experimental Staphylococcus aureusEndocarditis Through Antiplatelet and Antibacterial Effects. Circulation. 1999;99:2791-2797.
7. Bayer A, Cheung A, Gemery J, Sedlacek M, Remillard B. Aspirin Treatment Is
Associated With a Significantly Decreased Risk of staphylococcus aureus Bacteria in
Hemodialusis Patients With Tunneled Catheters. National Kidney Foundation 2007;
401-408.
8. Cunha Burke A, Domenico Philip, Hopkins Terence.The effect of sodium salicylate
on antibiotic susceptibility and synergy in Klebsiella pneumoniae. Journal of
Antimicrobial Chemotherapy (1990) 26, 343-351.
9. E John, Graham E. James, Muthaijan Arunachalam, Price C.T, Riordan T.James,
Voorhies Van Wayne, and Wilkinson J. Brian. Response of Staphylococcus to
Salicylate Challenge. Journal of Bacteriology, 189(1), 220-227.
10. Fakih M, Hanna M, Johnson L, Khosrovaneh A, Riederer K, Saeed S, Tabriz S, Shah A, Sharma M. Reduced Vancomycin Susceptibility and Heterogeneous Subpopulation in Persistent or Recurrent Methicillin‐Resistant Staphylococcus aureus Bacteremia. Clinical Infectious Diseases 2004;38:1328–1330.
11. Lewis Kim, Salyers A. Abigail, TaberH.W., Wax G. Richard. Bacterial resistance to
antimicrobials.New York, NY: Marcel Dekker Inc.0-8247-0635-8.
12. Mahesh B. K. Bandera, et. al, (2006). Salycilic acid reduces the Production of
Several potential Virulence Factors of Pseudomonas aeruginosa associated with
Microbial Keratitis. Investigative Ophthalmology and Visual Science.
2006;47:4453-4460.
13. Marangos M N, Nicolau D P, Nightingale C H,Quintiliani R. Influence of aspirin on
development and treatment of experimental Staphylococcus aureus endocarditis.
Antimicrob Agents Chemother. 1995 August; 39(8): 1748–1751.
14. W H Wang, et al.(2003).Aspirin inhibits the growth of Helicobacter-pylori and
enhance its suceptability to antimicrobial agent. GUT an international journal of
Gasteroenterology and Hepatology. 2003 Apr;52(4):490-5.
Formatting is incorrect on all sources, LastName, Intitial.Initial. You never put et al in your literature cited, list out every author. Should go in ascending alphabetical order by the 1st author’s last name. No numbering also – I’m sure Teh told you that once already this semester on your initial and final project proposals Sarai.
Review Form
Department of Biological Sciences
SaddlebackCollege, Mission Viejo, CA92692
Author (s):Finks and Sabet
Title:Response of Staphylococcus aureus to acetylsalicylate challenge while in the presence of Notatum Penicillium
Summary
Summarize the paper succinctly and dispassionately. Do not criticize here, just show that you understood the paper.
The paper was somewhat confusing with all the scientific names but what I understood of it was that the authors were looking to see if there was a difference between growth of Staphylococcus aureus and Notatum Penicillium in the presence of aspirin. They used agar plates and incubated them for a period of three days then measured the growth of each agar plate by calculating the diameter. Their results showed that there was a significant difference between all four groups. In the discussion they then explained what could have caused the differences between the groups and possible errors that could have been made.
General Comments
Generally explain the paper’s strengths and weaknesses and whether they are serious, or important to our current state of knowledge.
This paper is strong in its introduction by explaining sufficient background of their topic and previous studies done related to their project. It is also strong in the materials and methods where they described what procedures were done and what materials were used and how they prepared those materials.
This paper is weak in notation of the scientific names and its title. The scientific names were not notated correctly, they need to be fixed and italicized correctly. The title includes the word challenge after acetylsalicylate which is not defined nor mentioned again throughout the paper.
The weaknesses aren’t too serious but it is important to correct the errors they had.
Technical Criticism
Review technical issues, organization and clarity. Provide a table of typographical errors, grammatical errors, and minor textual problems. It's not the reviewer's job to copy Edit the paper, mark the manuscript.
This paper was a final versionThis paper was a rough draft
This paper was well organized but the clarity needs some work. The scientific names of the bacteria were not written correctly. The descriptions of each bacteria used needs to be clarified.