Module 1

Etudes

Module 1: Bacterial Pathogenesis
Laboratory report 1
Carriage of Opportunistic Bacterial Pathogens – weekS 2-5
-121285191771To determine the carriage rate of Methicillin-resistant Staphylococcus aureus (MRSA) in a population and determine its virulence properties.
0To determine the carriage rate of Methicillin-resistant Staphylococcus aureus (MRSA) in a population and determine its virulence properties.
What was the aim of your investigation? (1-2 sentences)
-125715200424A nasal sample was taken and a homogenous suspension was created using saline solution. The suspension was cultured using a 16-streak technique onto three different media types (horse blood agar, mannitol salt agar and colistin nalidixic acid agar) chosen for their selective or differential properties. Control plates were also prepared on the same agars with Staphylococcus aureus and Streptococcus pneumoniae. The control plates were used for comparison to the sample plates. From the nasal sample taken S. aureus was not isolated and a control sample was used for the rest of the experiments. A DNase test was undertaken by creating a single 3-4cm streak down the centre of the agar plate. Post incubation this plate was flooded with hydrochloric acid and incubated at room temperature for one minute. The hydrochloric acid was removed and the plate was examined on a dark surface for any clearing. A coagulase test was undertaken to determine if the sample was MRSA positive. If the sample clumps or agglutinates then the sample is positive. Lastly a cefoxitin disc test was undertaken to determine if the sample isolated was MRSA. A 107 CFU/suspension was made using a S. aureus sample and saline. The suspension was then lawn inoculated onto a Mueller Hinton agar +2% sodium chloride plate. The cefoxitin disc was placed in the centre of the plate and incubated. Post incubation the zone of inhibition was measured to determine if it was cefoxitin resistant and potentially an MRSA strain. 0A nasal sample was taken and a homogenous suspension was created using saline solution. The suspension was cultured using a 16-streak technique onto three different media types (horse blood agar, mannitol salt agar and colistin nalidixic acid agar) chosen for their selective or differential properties. Control plates were also prepared on the same agars with Staphylococcus aureus and Streptococcus pneumoniae. The control plates were used for comparison to the sample plates. From the nasal sample taken S. aureus was not isolated and a control sample was used for the rest of the experiments. A DNase test was undertaken by creating a single 3-4cm streak down the centre of the agar plate. Post incubation this plate was flooded with hydrochloric acid and incubated at room temperature for one minute. The hydrochloric acid was removed and the plate was examined on a dark surface for any clearing. A coagulase test was undertaken to determine if the sample was MRSA positive. If the sample clumps or agglutinates then the sample is positive. Lastly a cefoxitin disc test was undertaken to determine if the sample isolated was MRSA. A 107 CFU/suspension was made using a S. aureus sample and saline. The suspension was then lawn inoculated onto a Mueller Hinton agar +2% sodium chloride plate. The cefoxitin disc was placed in the centre of the plate and incubated. Post incubation the zone of inhibition was measured to determine if it was cefoxitin resistant and potentially an MRSA strain. Briefly summarise the methods and describe their purpose in addressing the aim(1/4 page)
-390916171791Table 1: Macroscopic identification of samples and observations in regards to different media types
Sample Size Colour Opaque Shape Edge Elevation Coverage Other/ Notes
S. aureus control MSA media Very small (less than 0.5mm) White
cream opaque round entire Slight ++++ Turned media bright yellow= fermentation of mannitol
HBA media small White/grey opaque round entire slight ++++ Poorly isolated bacteria
CNA media Small (1mm) White/grey opaque round entire Slight
++++ –
S. pneumoniae MSA media – – – – – – – No bacteria grew
HBA media Small (1mm) Brown/pale yellow opaque round entire slight +++ Green area around/underneath the bacteria=
Alpha haemolysis
CNA media Small (1mm) Brown/pale yellow opaque round entire Slight
Barely-mostly flat ++ Green area around/underneath the bacteria=
Alpha haemolysis
Sample MSA media – – – – – – – No bacteria grew
HBA media Largish
(1.5mm) white opaque round entire slight + Very few bacteria grew
CNA media – – – – – – – No bacteria grew

Figure 1: Results from Coagulase and Cefoxitin Disc Tests Within a Student Population to Determine the MRSA Carriage Rate. In the population of students studied, there was 33% MRSA positive samples determined using the cefoxitin disc test. The sample was deemed MRSA positive if the zone of inhibition was 16mm or more. All other samples were deemed MRSA negative (67%). The coagulase test indicated the percentage of the population with coagulase positive S. aureus. In this population only 31% of samples were positive and 69% were negative for the coagulase test.
00Table 1: Macroscopic identification of samples and observations in regards to different media types
Sample Size Colour Opaque Shape Edge Elevation Coverage Other/ Notes
S. aureus control MSA media Very small (less than 0.5mm) White
cream opaque round entire Slight ++++ Turned media bright yellow= fermentation of mannitol
HBA media small White/grey opaque round entire slight ++++ Poorly isolated bacteria
CNA media Small (1mm) White/grey opaque round entire Slight
++++ –
S. pneumoniae MSA media – – – – – – – No bacteria grew
HBA media Small (1mm) Brown/pale yellow opaque round entire slight +++ Green area around/underneath the bacteria=
Alpha haemolysis
CNA media Small (1mm) Brown/pale yellow opaque round entire Slight
Barely-mostly flat ++ Green area around/underneath the bacteria=
Alpha haemolysis
Sample MSA media – – – – – – – No bacteria grew
HBA media Largish
(1.5mm) white opaque round entire slight + Very few bacteria grew
CNA media – – – – – – – No bacteria grew

Figure 1: Results from Coagulase and Cefoxitin Disc Tests Within a Student Population to Determine the MRSA Carriage Rate. In the population of students studied, there was 33% MRSA positive samples determined using the cefoxitin disc test. The sample was deemed MRSA positive if the zone of inhibition was 16mm or more. All other samples were deemed MRSA negative (67%). The coagulase test indicated the percentage of the population with coagulase positive S. aureus. In this population only 31% of samples were positive and 69% were negative for the coagulase test.

Report your results and findings. (1/2 – 1 page)
Conclusions (2-3 sentences)
-7865841671In the studied population only 15 people (13%) were carriers of S. aureus in the nasal region with 33% of carriers having MRSA positive samples. 31% of the studied population also carried the virulent coagulase positive variation of S. aureus. The results may be skewed as the number of carriers recorded for the carriage rate tests (coagulase test and cefoxitin disc test) were inconsistent.
0In the studied population only 15 people (13%) were carriers of S. aureus in the nasal region with 33% of carriers having MRSA positive samples. 31% of the studied population also carried the virulent coagulase positive variation of S. aureus. The results may be skewed as the number of carriers recorded for the carriage rate tests (coagulase test and cefoxitin disc test) were inconsistent.

Discussion of results in relation to pathogenesis. (3/4-page total; 2-4 sentences for each answer)
(this will be based on independent or laboratory/workshop-directed research you have performed)
-104450342191For a carrier to become infected with MRSA the host has to trigger the opportunistic nature of this bacteria and cause the upregulation of virulence genes ADDIN EN.CITE <EndNote><Cite><Author>Liu</Author><Year>2009</Year><RecNum>32</RecNum><DisplayText>(2)</DisplayText><record><rec-number>32</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536463322″>32</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Liu, George Y.</author></authors></contributors><titles><title>Molecular Pathogenesis of Staphylococcus aureus Infection</title><secondary-title>Pediatric research</secondary-title></titles><periodical><full-title>Pediatric research</full-title></periodical><pages>71R-77R</pages><volume>65</volume><number>5 Pt 2</number><dates><year>2009</year></dates><isbn>0031-3998 1530-0447</isbn><accession-num>PMC2919328</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2919328/</url></related-urls></urls><electronic-resource-num>10.1203/PDR.0b013e31819dc44d</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(1). The bacteria has to firstly outcompete the other resident flora and become the dominant bacteria in the niche ADDIN EN.CITE <EndNote><Cite><Author>Liu</Author><Year>2009</Year><RecNum>32</RecNum><DisplayText>(2)</DisplayText><record><rec-number>32</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536463322″>32</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Liu, George Y.</author></authors></contributors><titles><title>Molecular Pathogenesis of Staphylococcus aureus Infection</title><secondary-title>Pediatric research</secondary-title></titles><periodical><full-title>Pediatric research</full-title></periodical><pages>71R-77R</pages><volume>65</volume><number>5 Pt 2</number><dates><year>2009</year></dates><isbn>0031-3998 1530-0447</isbn><accession-num>PMC2919328</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2919328/</url></related-urls></urls><electronic-resource-num>10.1203/PDR.0b013e31819dc44d</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(1). The alternate way for a carrier to become infected is if the bacteria is moved to a region of the body it did not previously occupy. This may occur via wounds or other methods of infection.

0For a carrier to become infected with MRSA the host has to trigger the opportunistic nature of this bacteria and cause the upregulation of virulence genes ADDIN EN.CITE <EndNote><Cite><Author>Liu</Author><Year>2009</Year><RecNum>32</RecNum><DisplayText>(2)</DisplayText><record><rec-number>32</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536463322″>32</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Liu, George Y.</author></authors></contributors><titles><title>Molecular Pathogenesis of Staphylococcus aureus Infection</title><secondary-title>Pediatric research</secondary-title></titles><periodical><full-title>Pediatric research</full-title></periodical><pages>71R-77R</pages><volume>65</volume><number>5 Pt 2</number><dates><year>2009</year></dates><isbn>0031-3998 1530-0447</isbn><accession-num>PMC2919328</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2919328/</url></related-urls></urls><electronic-resource-num>10.1203/PDR.0b013e31819dc44d</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(1). The bacteria has to firstly outcompete the other resident flora and become the dominant bacteria in the niche ADDIN EN.CITE <EndNote><Cite><Author>Liu</Author><Year>2009</Year><RecNum>32</RecNum><DisplayText>(2)</DisplayText><record><rec-number>32</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536463322″>32</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Liu, George Y.</author></authors></contributors><titles><title>Molecular Pathogenesis of Staphylococcus aureus Infection</title><secondary-title>Pediatric research</secondary-title></titles><periodical><full-title>Pediatric research</full-title></periodical><pages>71R-77R</pages><volume>65</volume><number>5 Pt 2</number><dates><year>2009</year></dates><isbn>0031-3998 1530-0447</isbn><accession-num>PMC2919328</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2919328/</url></related-urls></urls><electronic-resource-num>10.1203/PDR.0b013e31819dc44d</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(1). The alternate way for a carrier to become infected is if the bacteria is moved to a region of the body it did not previously occupy. This may occur via wounds or other methods of infection.

QUESTION 1: Explain two factors necessary for MRSA infection to occur in individuals who carriers of this bacterium are.

-125715204528Microbial surface components recognising adhesive matrix molecules (MSCRAMMs) play a role in the colonisation of new, unknown environments ADDIN EN.CITE <EndNote><Cite><Author>Belkum</Author><Year>2011</Year><RecNum>29</RecNum><DisplayText>(4)</DisplayText><record><rec-number>29</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1535946760″>29</key></foreign-keys><ref-type name=”Book Section”>5</ref-type><contributors><authors><author>Alex van Belkum</author></authors><secondary-authors><author>Curtis, Nigel</author><author>Finn, Adam</author><author>Pollard, Andrew J.</author></secondary-authors></contributors><titles><title>Novel Technology to Study Co-Evolution of Humans and Staphylococcus aureus: Consequences for Interpreting the Biology of Colonisation and Infection</title><secondary-title>Hot Topics in Infection and Immunity in Children VII</secondary-title></titles><pages>273-288</pages><dates><year>2011</year></dates><pub-location>New York, NY</pub-location><publisher>Springer New York</publisher><isbn>978-1-4419-7185-2</isbn><label>van Belkum2011</label><urls><related-urls><url>https://doi.org/10.1007/978-1-4419-7185-2_19</url></related-urls></urls><electronic-resource-num>10.1007/978-1-4419-7185-2_19</electronic-resource-num><access-date>29/08/18</access-date></record></Cite></EndNote>(2). MSCRAMMs form a category of proteins which facilitate colonisation by recognition of a range of diversely different molecules ADDIN EN.CITE <EndNote><Cite><Author>Belkum</Author><Year>2011</Year><RecNum>29</RecNum><DisplayText>(4)</DisplayText><record><rec-number>29</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1535946760″>29</key></foreign-keys><ref-type name=”Book Section”>5</ref-type><contributors><authors><author>Alex van Belkum</author></authors><secondary-authors><author>Curtis, Nigel</author><author>Finn, Adam</author><author>Pollard, Andrew J.</author></secondary-authors></contributors><titles><title>Novel Technology to Study Co-Evolution of Humans and Staphylococcus aureus: Consequences for Interpreting the Biology of Colonisation and Infection</title><secondary-title>Hot Topics in Infection and Immunity in Children VII</secondary-title></titles><pages>273-288</pages><dates><year>2011</year></dates><pub-location>New York, NY</pub-location><publisher>Springer New York</publisher><isbn>978-1-4419-7185-2</isbn><label>van Belkum2011</label><urls><related-urls><url>https://doi.org/10.1007/978-1-4419-7185-2_19</url></related-urls></urls><electronic-resource-num>10.1007/978-1-4419-7185-2_19</electronic-resource-num><access-date>29/08/18</access-date></record></Cite></EndNote>(2). Generally speaking, MSCRAMMs bind to the heterodimeric human glycoprotein fibronectin which allows the pathogen to both colonise and potentially exploit physiological functions to aid in invasion PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5MaWFuZzwvQXV0aG9yPjxZZWFyPjIwMTY8L1llYXI+PFJl
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ADDIN EN.CITE.DATA (3). Once the bacteria has made its way into the body it has to then avoid the host immune functions, so that it is not removed. S.aureus flourishes in the nasal cavity due to the lack of defences found ADDIN EN.CITE <EndNote><Cite><Author>Kluytmans</Author><Year>1997</Year><RecNum>37</RecNum><DisplayText>(11)</DisplayText><record><rec-number>37</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536546427″>37</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Kluytmans, J.</author><author>van Belkum, A.</author><author>Verbrugh, H.</author></authors></contributors><auth-address>Ignatius Hospital Breda, The Netherlands.</auth-address><titles><title>Nasal carriage of Staphylococcus aureus: epidemiology, underlying mechanisms, and associated risks</title><secondary-title>Clin Microbiol Rev</secondary-title><alt-title>Clinical microbiology reviews</alt-title></titles><periodical><full-title>Clin Microbiol Rev</full-title><abbr-1>Clinical microbiology reviews</abbr-1></periodical><alt-periodical><full-title>Clin Microbiol Rev</full-title><abbr-1>Clinical microbiology reviews</abbr-1></alt-periodical><pages>505-20</pages><volume>10</volume><number>3</number><edition>1997/07/01</edition><keywords><keyword>Bacterial Adhesion</keyword><keyword>Carrier State/epidemiology/*microbiology/prevention &amp; control</keyword><keyword>Endothelium</keyword><keyword>Endothelium, Corneal</keyword><keyword>Epithelium</keyword><keyword>HIV Infections/complications</keyword><keyword>Humans</keyword><keyword>Peritoneal Dialysis, Continuous Ambulatory</keyword><keyword>Renal Dialysis</keyword><keyword>Risk Factors</keyword><keyword>*Staphylococcal Infections/epidemiology/etiology/prevention &amp; control</keyword><keyword>*Staphylococcus aureus/pathogenicity/physiology</keyword><keyword>Surgical Wound Infection/microbiology</keyword></keywords><dates><year>1997</year><pub-dates><date>Jul</date></pub-dates></dates><isbn>0893-8512 (Print) 0893-8512</isbn><accession-num>9227864</accession-num><urls></urls><custom2>PMC172932</custom2><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(4).

0Microbial surface components recognising adhesive matrix molecules (MSCRAMMs) play a role in the colonisation of new, unknown environments ADDIN EN.CITE <EndNote><Cite><Author>Belkum</Author><Year>2011</Year><RecNum>29</RecNum><DisplayText>(4)</DisplayText><record><rec-number>29</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1535946760″>29</key></foreign-keys><ref-type name=”Book Section”>5</ref-type><contributors><authors><author>Alex van Belkum</author></authors><secondary-authors><author>Curtis, Nigel</author><author>Finn, Adam</author><author>Pollard, Andrew J.</author></secondary-authors></contributors><titles><title>Novel Technology to Study Co-Evolution of Humans and Staphylococcus aureus: Consequences for Interpreting the Biology of Colonisation and Infection</title><secondary-title>Hot Topics in Infection and Immunity in Children VII</secondary-title></titles><pages>273-288</pages><dates><year>2011</year></dates><pub-location>New York, NY</pub-location><publisher>Springer New York</publisher><isbn>978-1-4419-7185-2</isbn><label>van Belkum2011</label><urls><related-urls><url>https://doi.org/10.1007/978-1-4419-7185-2_19</url></related-urls></urls><electronic-resource-num>10.1007/978-1-4419-7185-2_19</electronic-resource-num><access-date>29/08/18</access-date></record></Cite></EndNote>(2). MSCRAMMs form a category of proteins which facilitate colonisation by recognition of a range of diversely different molecules ADDIN EN.CITE <EndNote><Cite><Author>Belkum</Author><Year>2011</Year><RecNum>29</RecNum><DisplayText>(4)</DisplayText><record><rec-number>29</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1535946760″>29</key></foreign-keys><ref-type name=”Book Section”>5</ref-type><contributors><authors><author>Alex van Belkum</author></authors><secondary-authors><author>Curtis, Nigel</author><author>Finn, Adam</author><author>Pollard, Andrew J.</author></secondary-authors></contributors><titles><title>Novel Technology to Study Co-Evolution of Humans and Staphylococcus aureus: Consequences for Interpreting the Biology of Colonisation and Infection</title><secondary-title>Hot Topics in Infection and Immunity in Children VII</secondary-title></titles><pages>273-288</pages><dates><year>2011</year></dates><pub-location>New York, NY</pub-location><publisher>Springer New York</publisher><isbn>978-1-4419-7185-2</isbn><label>van Belkum2011</label><urls><related-urls><url>https://doi.org/10.1007/978-1-4419-7185-2_19</url></related-urls></urls><electronic-resource-num>10.1007/978-1-4419-7185-2_19</electronic-resource-num><access-date>29/08/18</access-date></record></Cite></EndNote>(2). Generally speaking, MSCRAMMs bind to the heterodimeric human glycoprotein fibronectin which allows the pathogen to both colonise and potentially exploit physiological functions to aid in invasion PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5MaWFuZzwvQXV0aG9yPjxZZWFyPjIwMTY8L1llYXI+PFJl
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ADDIN EN.CITE.DATA (3). Once the bacteria has made its way into the body it has to then avoid the host immune functions, so that it is not removed. S.aureus flourishes in the nasal cavity due to the lack of defences found ADDIN EN.CITE <EndNote><Cite><Author>Kluytmans</Author><Year>1997</Year><RecNum>37</RecNum><DisplayText>(11)</DisplayText><record><rec-number>37</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536546427″>37</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Kluytmans, J.</author><author>van Belkum, A.</author><author>Verbrugh, H.</author></authors></contributors><auth-address>Ignatius Hospital Breda, The Netherlands.</auth-address><titles><title>Nasal carriage of Staphylococcus aureus: epidemiology, underlying mechanisms, and associated risks</title><secondary-title>Clin Microbiol Rev</secondary-title><alt-title>Clinical microbiology reviews</alt-title></titles><periodical><full-title>Clin Microbiol Rev</full-title><abbr-1>Clinical microbiology reviews</abbr-1></periodical><alt-periodical><full-title>Clin Microbiol Rev</full-title><abbr-1>Clinical microbiology reviews</abbr-1></alt-periodical><pages>505-20</pages><volume>10</volume><number>3</number><edition>1997/07/01</edition><keywords><keyword>Bacterial Adhesion</keyword><keyword>Carrier State/epidemiology/*microbiology/prevention &amp; control</keyword><keyword>Endothelium</keyword><keyword>Endothelium, Corneal</keyword><keyword>Epithelium</keyword><keyword>HIV Infections/complications</keyword><keyword>Humans</keyword><keyword>Peritoneal Dialysis, Continuous Ambulatory</keyword><keyword>Renal Dialysis</keyword><keyword>Risk Factors</keyword><keyword>*Staphylococcal Infections/epidemiology/etiology/prevention &amp; control</keyword><keyword>*Staphylococcus aureus/pathogenicity/physiology</keyword><keyword>Surgical Wound Infection/microbiology</keyword></keywords><dates><year>1997</year><pub-dates><date>Jul</date></pub-dates></dates><isbn>0893-8512 (Print) 0893-8512</isbn><accession-num>9227864</accession-num><urls></urls><custom2>PMC172932</custom2><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(4).

QUESTION 2: Describe two molecular determinants required for S. aureus to colonise and survive in the nose.

-123190181610Methicillin resistance is expressed due to a mecI-mediated repression through a mutation which allows the strain to become resistant ADDIN EN.CITE <EndNote><Cite><Author>Appelbaum</Author><Year>2007</Year><RecNum>31</RecNum><DisplayText>(8)</DisplayText><record><rec-number>31</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536459837″>31</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Appelbaum, P. C.</author></authors></contributors><auth-address>Division of Clinical Pathology, Penn State College of Medicine, and Clinical Microbiology, Penn State Milton S. Hershey Medical Center, Hershey, PA 17033, USA. [email protected]</auth-address><titles><title>Microbiology of antibiotic resistance in Staphylococcus aureus</title><secondary-title>Clin Infect Dis</secondary-title><alt-title>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</alt-title></titles><periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></periodical><alt-periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></alt-periodical><pages>S165-70</pages><volume>45 Suppl 3</volume><edition>2007/09/19</edition><keywords><keyword>Anti-Bacterial Agents/*pharmacology</keyword><keyword>Drug Resistance, Multiple, Bacterial/*physiology</keyword><keyword>Humans</keyword><keyword>Selection, Genetic</keyword><keyword>Soft Tissue Infections/epidemiology/microbiology</keyword><keyword>Staphylococcal Infections/epidemiology/*microbiology</keyword><keyword>Staphylococcus aureus/*drug effects/*physiology</keyword></keywords><dates><year>2007</year><pub-dates><date>Sep 15</date></pub-dates></dates><isbn>1058-4838</isbn><accession-num>17712742</accession-num><urls></urls><electronic-resource-num>10.1086/519474</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(5). In pre-MRSA bacteria the mecA gene (located on the SCCmec cassette) and its regulator genes mecI and mecR1 do not express resistance ADDIN EN.CITE <EndNote><Cite><Author>Appelbaum</Author><Year>2007</Year><RecNum>31</RecNum><DisplayText>(8)</DisplayText><record><rec-number>31</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536459837″>31</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Appelbaum, P. C.</author></authors></contributors><auth-address>Division of Clinical Pathology, Penn State College of Medicine, and Clinical Microbiology, Penn State Milton S. Hershey Medical Center, Hershey, PA 17033, USA. [email protected]</auth-address><titles><title>Microbiology of antibiotic resistance in Staphylococcus aureus</title><secondary-title>Clin Infect Dis</secondary-title><alt-title>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</alt-title></titles><periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></periodical><alt-periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></alt-periodical><pages>S165-70</pages><volume>45 Suppl 3</volume><edition>2007/09/19</edition><keywords><keyword>Anti-Bacterial Agents/*pharmacology</keyword><keyword>Drug Resistance, Multiple, Bacterial/*physiology</keyword><keyword>Humans</keyword><keyword>Selection, Genetic</keyword><keyword>Soft Tissue Infections/epidemiology/microbiology</keyword><keyword>Staphylococcal Infections/epidemiology/*microbiology</keyword><keyword>Staphylococcus aureus/*drug effects/*physiology</keyword></keywords><dates><year>2007</year><pub-dates><date>Sep 15</date></pub-dates></dates><isbn>1058-4838</isbn><accession-num>17712742</accession-num><urls></urls><electronic-resource-num>10.1086/519474</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(5). Some SCCmec cassettes can carry additional genetic elements that confer resistance to different antibiotic classes such as tetracyclines ADDIN EN.CITE <EndNote><Cite><Author>Appelbaum</Author><Year>2007</Year><RecNum>31</RecNum><DisplayText>(8)</DisplayText><record><rec-number>31</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536459837″>31</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Appelbaum, P. C.</author></authors></contributors><auth-address>Division of Clinical Pathology, Penn State College of Medicine, and Clinical Microbiology, Penn State Milton S. Hershey Medical Center, Hershey, PA 17033, USA. [email protected]</auth-address><titles><title>Microbiology of antibiotic resistance in Staphylococcus aureus</title><secondary-title>Clin Infect Dis</secondary-title><alt-title>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</alt-title></titles><periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></periodical><alt-periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></alt-periodical><pages>S165-70</pages><volume>45 Suppl 3</volume><edition>2007/09/19</edition><keywords><keyword>Anti-Bacterial Agents/*pharmacology</keyword><keyword>Drug Resistance, Multiple, Bacterial/*physiology</keyword><keyword>Humans</keyword><keyword>Selection, Genetic</keyword><keyword>Soft Tissue Infections/epidemiology/microbiology</keyword><keyword>Staphylococcal Infections/epidemiology/*microbiology</keyword><keyword>Staphylococcus aureus/*drug effects/*physiology</keyword></keywords><dates><year>2007</year><pub-dates><date>Sep 15</date></pub-dates></dates><isbn>1058-4838</isbn><accession-num>17712742</accession-num><urls></urls><electronic-resource-num>10.1086/519474</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(5). Cefoxitin has been correlated with the presence of mecA-mediated oxacillin resistance ADDIN EN.CITE <EndNote><Cite><Author>Appelbaum</Author><Year>2007</Year><RecNum>31</RecNum><DisplayText>(8)</DisplayText><record><rec-number>31</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536459837″>31</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Appelbaum, P. C.</author></authors></contributors><auth-address>Division of Clinical Pathology, Penn State College of Medicine, and Clinical Microbiology, Penn State Milton S. Hershey Medical Center, Hershey, PA 17033, USA. [email protected]</auth-address><titles><title>Microbiology of antibiotic resistance in Staphylococcus aureus</title><secondary-title>Clin Infect Dis</secondary-title><alt-title>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</alt-title></titles><periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></periodical><alt-periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></alt-periodical><pages>S165-70</pages><volume>45 Suppl 3</volume><edition>2007/09/19</edition><keywords><keyword>Anti-Bacterial Agents/*pharmacology</keyword><keyword>Drug Resistance, Multiple, Bacterial/*physiology</keyword><keyword>Humans</keyword><keyword>Selection, Genetic</keyword><keyword>Soft Tissue Infections/epidemiology/microbiology</keyword><keyword>Staphylococcal Infections/epidemiology/*microbiology</keyword><keyword>Staphylococcus aureus/*drug effects/*physiology</keyword></keywords><dates><year>2007</year><pub-dates><date>Sep 15</date></pub-dates></dates><isbn>1058-4838</isbn><accession-num>17712742</accession-num><urls></urls><electronic-resource-num>10.1086/519474</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(5).
0Methicillin resistance is expressed due to a mecI-mediated repression through a mutation which allows the strain to become resistant ADDIN EN.CITE <EndNote><Cite><Author>Appelbaum</Author><Year>2007</Year><RecNum>31</RecNum><DisplayText>(8)</DisplayText><record><rec-number>31</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536459837″>31</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Appelbaum, P. C.</author></authors></contributors><auth-address>Division of Clinical Pathology, Penn State College of Medicine, and Clinical Microbiology, Penn State Milton S. Hershey Medical Center, Hershey, PA 17033, USA. [email protected]</auth-address><titles><title>Microbiology of antibiotic resistance in Staphylococcus aureus</title><secondary-title>Clin Infect Dis</secondary-title><alt-title>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</alt-title></titles><periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></periodical><alt-periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></alt-periodical><pages>S165-70</pages><volume>45 Suppl 3</volume><edition>2007/09/19</edition><keywords><keyword>Anti-Bacterial Agents/*pharmacology</keyword><keyword>Drug Resistance, Multiple, Bacterial/*physiology</keyword><keyword>Humans</keyword><keyword>Selection, Genetic</keyword><keyword>Soft Tissue Infections/epidemiology/microbiology</keyword><keyword>Staphylococcal Infections/epidemiology/*microbiology</keyword><keyword>Staphylococcus aureus/*drug effects/*physiology</keyword></keywords><dates><year>2007</year><pub-dates><date>Sep 15</date></pub-dates></dates><isbn>1058-4838</isbn><accession-num>17712742</accession-num><urls></urls><electronic-resource-num>10.1086/519474</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(5). In pre-MRSA bacteria the mecA gene (located on the SCCmec cassette) and its regulator genes mecI and mecR1 do not express resistance ADDIN EN.CITE <EndNote><Cite><Author>Appelbaum</Author><Year>2007</Year><RecNum>31</RecNum><DisplayText>(8)</DisplayText><record><rec-number>31</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536459837″>31</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Appelbaum, P. C.</author></authors></contributors><auth-address>Division of Clinical Pathology, Penn State College of Medicine, and Clinical Microbiology, Penn State Milton S. Hershey Medical Center, Hershey, PA 17033, USA. [email protected]</auth-address><titles><title>Microbiology of antibiotic resistance in Staphylococcus aureus</title><secondary-title>Clin Infect Dis</secondary-title><alt-title>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</alt-title></titles><periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></periodical><alt-periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></alt-periodical><pages>S165-70</pages><volume>45 Suppl 3</volume><edition>2007/09/19</edition><keywords><keyword>Anti-Bacterial Agents/*pharmacology</keyword><keyword>Drug Resistance, Multiple, Bacterial/*physiology</keyword><keyword>Humans</keyword><keyword>Selection, Genetic</keyword><keyword>Soft Tissue Infections/epidemiology/microbiology</keyword><keyword>Staphylococcal Infections/epidemiology/*microbiology</keyword><keyword>Staphylococcus aureus/*drug effects/*physiology</keyword></keywords><dates><year>2007</year><pub-dates><date>Sep 15</date></pub-dates></dates><isbn>1058-4838</isbn><accession-num>17712742</accession-num><urls></urls><electronic-resource-num>10.1086/519474</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(5). Some SCCmec cassettes can carry additional genetic elements that confer resistance to different antibiotic classes such as tetracyclines ADDIN EN.CITE <EndNote><Cite><Author>Appelbaum</Author><Year>2007</Year><RecNum>31</RecNum><DisplayText>(8)</DisplayText><record><rec-number>31</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536459837″>31</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Appelbaum, P. C.</author></authors></contributors><auth-address>Division of Clinical Pathology, Penn State College of Medicine, and Clinical Microbiology, Penn State Milton S. Hershey Medical Center, Hershey, PA 17033, USA. [email protected]</auth-address><titles><title>Microbiology of antibiotic resistance in Staphylococcus aureus</title><secondary-title>Clin Infect Dis</secondary-title><alt-title>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</alt-title></titles><periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></periodical><alt-periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></alt-periodical><pages>S165-70</pages><volume>45 Suppl 3</volume><edition>2007/09/19</edition><keywords><keyword>Anti-Bacterial Agents/*pharmacology</keyword><keyword>Drug Resistance, Multiple, Bacterial/*physiology</keyword><keyword>Humans</keyword><keyword>Selection, Genetic</keyword><keyword>Soft Tissue Infections/epidemiology/microbiology</keyword><keyword>Staphylococcal Infections/epidemiology/*microbiology</keyword><keyword>Staphylococcus aureus/*drug effects/*physiology</keyword></keywords><dates><year>2007</year><pub-dates><date>Sep 15</date></pub-dates></dates><isbn>1058-4838</isbn><accession-num>17712742</accession-num><urls></urls><electronic-resource-num>10.1086/519474</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(5). Cefoxitin has been correlated with the presence of mecA-mediated oxacillin resistance ADDIN EN.CITE <EndNote><Cite><Author>Appelbaum</Author><Year>2007</Year><RecNum>31</RecNum><DisplayText>(8)</DisplayText><record><rec-number>31</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536459837″>31</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Appelbaum, P. C.</author></authors></contributors><auth-address>Division of Clinical Pathology, Penn State College of Medicine, and Clinical Microbiology, Penn State Milton S. Hershey Medical Center, Hershey, PA 17033, USA. [email protected]</auth-address><titles><title>Microbiology of antibiotic resistance in Staphylococcus aureus</title><secondary-title>Clin Infect Dis</secondary-title><alt-title>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</alt-title></titles><periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></periodical><alt-periodical><full-title>Clin Infect Dis</full-title><abbr-1>Clinical infectious diseases : an official publication of the Infectious Diseases Society of America</abbr-1></alt-periodical><pages>S165-70</pages><volume>45 Suppl 3</volume><edition>2007/09/19</edition><keywords><keyword>Anti-Bacterial Agents/*pharmacology</keyword><keyword>Drug Resistance, Multiple, Bacterial/*physiology</keyword><keyword>Humans</keyword><keyword>Selection, Genetic</keyword><keyword>Soft Tissue Infections/epidemiology/microbiology</keyword><keyword>Staphylococcal Infections/epidemiology/*microbiology</keyword><keyword>Staphylococcus aureus/*drug effects/*physiology</keyword></keywords><dates><year>2007</year><pub-dates><date>Sep 15</date></pub-dates></dates><isbn>1058-4838</isbn><accession-num>17712742</accession-num><urls></urls><electronic-resource-num>10.1086/519474</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(5).
QUESTION 3: What is the molecular mechanism and genetic basis for cefoxitin resistance in S. aureus?
-188692209550 ADDIN EN.REFLIST
1 Liu, G. Y. (2009). Molecular Pathogenesis of Staphylococcus aureus Infection. Pediatric research, 65(5 Pt 2), 71R-77R. doi:10.1203/PDR.0b013e31819dc44d
2 Belkum, A. v. (2011). Novel Technology to Study Co-Evolution of Humans and Staphylococcus aureus: Consequences for Interpreting the Biology of Colonisation and Infection. In N. Curtis, A. Finn, & A. J. Pollard (Eds.), Hot Topics in Infection and Immunity in Children VII (pp. 273-288). New York, NY: Springer New York.

3 Liang, X., Garcia, B. L., Visai, L., Prabhakaran, S., Meenan, N. A., Potts, J. R., . . . Hook, M. (2016). Allosteric Regulation of Fibronectin/alpha5beta1 Interaction by Fibronectin-Binding MSCRAMMs. PLoS One, 11(7), e0159118. doi:10.1371/journal.pone.0159118
4Kluytmans, J., van Belkum, A., & Verbrugh, H. (1997). Nasal carriage of Staphylococcus aureus: epidemiology, underlying mechanisms, and associated risks. Clin Microbiol Rev, 10(3), 505-520.
5 Appelbaum, P. C. (2007). Microbiology of antibiotic resistance in Staphylococcus aureus. Clin Infect Dis, 45 Suppl 3, S165-170. doi:10.1086/519474

0 ADDIN EN.REFLIST
1 Liu, G. Y. (2009). Molecular Pathogenesis of Staphylococcus aureus Infection. Pediatric research, 65(5 Pt 2), 71R-77R. doi:10.1203/PDR.0b013e31819dc44d
2 Belkum, A. v. (2011). Novel Technology to Study Co-Evolution of Humans and Staphylococcus aureus: Consequences for Interpreting the Biology of Colonisation and Infection. In N. Curtis, A. Finn, & A. J. Pollard (Eds.), Hot Topics in Infection and Immunity in Children VII (pp. 273-288). New York, NY: Springer New York.

3 Liang, X., Garcia, B. L., Visai, L., Prabhakaran, S., Meenan, N. A., Potts, J. R., . . . Hook, M. (2016). Allosteric Regulation of Fibronectin/alpha5beta1 Interaction by Fibronectin-Binding MSCRAMMs. PLoS One, 11(7), e0159118. doi:10.1371/journal.pone.0159118
4Kluytmans, J., van Belkum, A., & Verbrugh, H. (1997). Nasal carriage of Staphylococcus aureus: epidemiology, underlying mechanisms, and associated risks. Clin Microbiol Rev, 10(3), 505-520.
5 Appelbaum, P. C. (2007). Microbiology of antibiotic resistance in Staphylococcus aureus. Clin Infect Dis, 45 Suppl 3, S165-170. doi:10.1086/519474

References (1/4 page)

Module 1: Bacterial Pathogenesis
Laboratory report 2
Hospital Outbreak of Klebsiella pneumoniae – weekS 2-6
-123696185983To determine the routes of transmission of Klebsiellosis pneumoniae which is causing hospital acquired infections (HAIs) and prevent a possible outbreak. The ability to form a biofilm and produce Extended Spectrum Beta Lactamase (ESBL) will also be assessed.
0To determine the routes of transmission of Klebsiellosis pneumoniae which is causing hospital acquired infections (HAIs) and prevent a possible outbreak. The ability to form a biofilm and produce Extended Spectrum Beta Lactamase (ESBL) will also be assessed.
What was the aim of your investigation? (1-2 sentences)
-125715196200A biofilm assay was undertaken to determine if the bacteria present in each sample could form a biofilm. The formation of a biofilm indicated the bacteria had a thick capsular polysaccharide layer. The biofilm assay was then stained using crystal violet and quantified using a plate reader.Extended spectrum beta lactamase production tests were demonstrated to determine the ability to produce ESBLs. This was undertaken using an antibiotic resistance plate test. The zones of inhibition for all the samples and tested antibiotics was measured. A nigrosin stain was undertaken for each sample to test for the presence of a capsular polysaccharide. After the nigrosin stain was dry, crystal violet was applied and air dried (note: do not wash the stain off). The slides were then visualised using microscopy and samples which contained capsules were found. All stains were imaged. K. pneumoniae produces capsular polysaccharide and therefore any samples that contained a capsule have potentially be transmitted. Any sample with positive results in all testing areas are likely to be K. pneumoniae that was transmitted to the area it was found in.
0A biofilm assay was undertaken to determine if the bacteria present in each sample could form a biofilm. The formation of a biofilm indicated the bacteria had a thick capsular polysaccharide layer. The biofilm assay was then stained using crystal violet and quantified using a plate reader.Extended spectrum beta lactamase production tests were demonstrated to determine the ability to produce ESBLs. This was undertaken using an antibiotic resistance plate test. The zones of inhibition for all the samples and tested antibiotics was measured. A nigrosin stain was undertaken for each sample to test for the presence of a capsular polysaccharide. After the nigrosin stain was dry, crystal violet was applied and air dried (note: do not wash the stain off). The slides were then visualised using microscopy and samples which contained capsules were found. All stains were imaged. K. pneumoniae produces capsular polysaccharide and therefore any samples that contained a capsule have potentially be transmitted. Any sample with positive results in all testing areas are likely to be K. pneumoniae that was transmitted to the area it was found in.
Briefly summarise the methods and describe their purpose in addressing the aim(1/4 page)

-348999267689Table 1: Macroscopic identification of bacteria in different samples
Sample Size colour opaque shape edge elevation coverage Other
patient 1 Small Greyish white Opaque
Round Entire Slight +++ –
patient 2 Small Greyish white Opaque Round
Entire Slight +++ –
blood pressure cuff Small Greyish white Opaque Round Entire Slight +++ –
computer Small Greyish white Opaque Round Entire Slight +++ Beta-Haemolysis of HBA
sink Large Greyish white Opaque Round entire None +++ –
Table 2: Average optical density of samples taken from the biofilm formation assay
Sample Average optical density of sample
Patient 1 1.0805
Patient 2 1.13075
Sink sample 1.109
Computer sample 0.579
Blood pressure cuff sample 0.03
Klebsiella pneumoniae positive sample 0.0285
Table 3: Antibiotic resistance assay of samples to determine ESBL production
AMC- 60 KZ-30 W-5 F-200 NOR-10 AMP-25
Sink 9mm 5mm 0mm 7mm 13mm 0mm
Patient 1 6mm 2mm 0mm 3mm 6mm 0mm
Computer 6mm 0mm 14mm 8mm 10mm 1mm
Patient 2 7mm 4mm 0mm 3mm 7mm 0mm
Blood pressure cuff 8mm 2mm 0mm 4mm 8mm 0mm
00Table 1: Macroscopic identification of bacteria in different samples
Sample Size colour opaque shape edge elevation coverage Other
patient 1 Small Greyish white Opaque
Round Entire Slight +++ –
patient 2 Small Greyish white Opaque Round
Entire Slight +++ –
blood pressure cuff Small Greyish white Opaque Round Entire Slight +++ –
computer Small Greyish white Opaque Round Entire Slight +++ Beta-Haemolysis of HBA
sink Large Greyish white Opaque Round entire None +++ –
Table 2: Average optical density of samples taken from the biofilm formation assay
Sample Average optical density of sample
Patient 1 1.0805
Patient 2 1.13075
Sink sample 1.109
Computer sample 0.579
Blood pressure cuff sample 0.03
Klebsiella pneumoniae positive sample 0.0285
Table 3: Antibiotic resistance assay of samples to determine ESBL production
AMC- 60 KZ-30 W-5 F-200 NOR-10 AMP-25
Sink 9mm 5mm 0mm 7mm 13mm 0mm
Patient 1 6mm 2mm 0mm 3mm 6mm 0mm
Computer 6mm 0mm 14mm 8mm 10mm 1mm
Patient 2 7mm 4mm 0mm 3mm 7mm 0mm
Blood pressure cuff 8mm 2mm 0mm 4mm 8mm 0mm
Report your results and findings. (1/2 – 1 page)

Conclusions (2-3 sentences)
-7865841671The K. pneumoniae was likely to have been transmitted to patients via the blood pressure cuff. It has a similar morphology and antibiotic resistance when compared to the patient samples as well as being easily accessible for a patient. The only seen discrepancy is the biofilm assay results. The discrepancy should be considered and further testing would allow for a more accurate diagnosis of the route of transmission of K. pneumoniae.

0The K. pneumoniae was likely to have been transmitted to patients via the blood pressure cuff. It has a similar morphology and antibiotic resistance when compared to the patient samples as well as being easily accessible for a patient. The only seen discrepancy is the biofilm assay results. The discrepancy should be considered and further testing would allow for a more accurate diagnosis of the route of transmission of K. pneumoniae.

Discussion of results in relation to pathogenesis. (3/4 page total; 2-4 sentences for each answer)
(this will be based on independent or laboratory/workshop-directed research you have performed)
-178878337969For Klebsiella pneumoniae formation of a biofilm allows for infection to occur through routes such as catheters and other medical instruments ADDIN EN.CITE <EndNote><Cite><Author>Murphy</Author><Year>2012</Year><RecNum>34</RecNum><DisplayText>(7)</DisplayText><record><rec-number>34</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536542638″>34</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Murphy, C. N.</author><author>Clegg, S.</author></authors></contributors><auth-address>Department of Microbiology, University of Iowa College of Medicine, Iowa City, IA 52242, USA.</auth-address><titles><title>Klebsiella pneumoniae and type 3 fimbriae: nosocomial infection, regulation and biofilm formation</title><secondary-title>Future Microbiol</secondary-title><alt-title>Future microbiology</alt-title></titles><periodical><full-title>Future Microbiol</full-title><abbr-1>Future microbiology</abbr-1></periodical><alt-periodical><full-title>Future Microbiol</full-title><abbr-1>Future microbiology</abbr-1></alt-periodical><pages>991-1002</pages><volume>7</volume><number>8</number><edition>2012/08/24</edition><keywords><keyword>Biofilms/*growth &amp; development</keyword><keyword>Catheter-Related Infections</keyword><keyword>Community-Acquired Infections/microbiology</keyword><keyword>Cross Infection/*microbiology</keyword><keyword>Cyclic GMP/analogs &amp; derivatives/metabolism</keyword><keyword>Fimbriae, Bacterial/*metabolism</keyword><keyword>Gene Expression Regulation, Bacterial</keyword><keyword>Humans</keyword><keyword>Klebsiella Infections/*microbiology</keyword><keyword>Klebsiella pneumoniae/*pathogenicity/*physiology</keyword><keyword>Virulence Factors/metabolism</keyword></keywords><dates><year>2012</year><pub-dates><date>Aug</date></pub-dates></dates><isbn>1746-0913</isbn><accession-num>22913357</accession-num><urls></urls><electronic-resource-num>10.2217/fmb.12.74</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(1). Catheters with a biofilm on them are one of the largest causes of nosocomial infections, as bacteria can evade host defence mechanisms and isn’t flushed out when urination occurs ADDIN EN.CITE ;EndNote;;Cite;;Author;Murphy;/Author;;Year;2012;/Year;;RecNum;34;/RecNum;;DisplayText;(7);/DisplayText;;record;;rec-number;34;/rec-number;;foreign-keys;;key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536542638″;34;/key;;/foreign-keys;;ref-type name=”Journal Article”;17;/ref-type;;contributors;;authors;;author;Murphy, C. N.;/author;;author;Clegg, S.;/author;;/authors;;/contributors;;auth-address;Department of Microbiology, University of Iowa College of Medicine, Iowa City, IA 52242, USA.;/auth-address;;titles;;title;Klebsiella pneumoniae and type 3 fimbriae: nosocomial infection, regulation and biofilm formation;/title;;secondary-title;Future Microbiol;/secondary-title;;alt-title;Future microbiology;/alt-title;;/titles;;periodical;;full-title;Future Microbiol;/full-title;;abbr-1;Future microbiology;/abbr-1;;/periodical;;alt-periodical;;full-title;Future Microbiol;/full-title;;abbr-1;Future microbiology;/abbr-1;;/alt-periodical;;pages;991-1002;/pages;;volume;7;/volume;;number;8;/number;;edition;2012/08/24;/edition;;keywords;;keyword;Biofilms/*growth &amp; development</keyword><keyword>Catheter-Related Infections</keyword><keyword>Community-Acquired Infections/microbiology</keyword><keyword>Cross Infection/*microbiology</keyword><keyword>Cyclic GMP/analogs &amp; derivatives/metabolism</keyword><keyword>Fimbriae, Bacterial/*metabolism</keyword><keyword>Gene Expression Regulation, Bacterial</keyword><keyword>Humans</keyword><keyword>Klebsiella Infections/*microbiology</keyword><keyword>Klebsiella pneumoniae/*pathogenicity/*physiology</keyword><keyword>Virulence Factors/metabolism</keyword></keywords><dates><year>2012</year><pub-dates><date>Aug</date></pub-dates></dates><isbn>1746-0913</isbn><accession-num>22913357</accession-num><urls></urls><electronic-resource-num>10.2217/fmb.12.74</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(1). The surface expression of type 3 fimbriae in K. pneumoniae is an indicator of biofilm formation abilities, as these appendages mediate the initiation and colonisation and growth of biofilms ADDIN EN.CITE <EndNote><Cite><Author>Murphy</Author><Year>2012</Year><RecNum>34</RecNum><DisplayText>(7)</DisplayText><record><rec-number>34</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536542638″>34</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Murphy, C. N.</author><author>Clegg, S.</author></authors></contributors><auth-address>Department of Microbiology, University of Iowa College of Medicine, Iowa City, IA 52242, USA.</auth-address><titles><title>Klebsiella pneumoniae and type 3 fimbriae: nosocomial infection, regulation and biofilm formation</title><secondary-title>Future Microbiol</secondary-title><alt-title>Future microbiology</alt-title></titles><periodical><full-title>Future Microbiol</full-title><abbr-1>Future microbiology</abbr-1></periodical><alt-periodical><full-title>Future Microbiol</full-title><abbr-1>Future microbiology</abbr-1></alt-periodical><pages>991-1002</pages><volume>7</volume><number>8</number><edition>2012/08/24</edition><keywords><keyword>Biofilms/*growth &amp; development</keyword><keyword>Catheter-Related Infections</keyword><keyword>Community-Acquired Infections/microbiology</keyword><keyword>Cross Infection/*microbiology</keyword><keyword>Cyclic GMP/analogs &amp; derivatives/metabolism</keyword><keyword>Fimbriae, Bacterial/*metabolism</keyword><keyword>Gene Expression Regulation, Bacterial</keyword><keyword>Humans</keyword><keyword>Klebsiella Infections/*microbiology</keyword><keyword>Klebsiella pneumoniae/*pathogenicity/*physiology</keyword><keyword>Virulence Factors/metabolism</keyword></keywords><dates><year>2012</year><pub-dates><date>Aug</date></pub-dates></dates><isbn>1746-0913</isbn><accession-num>22913357</accession-num><urls></urls><electronic-resource-num>10.2217/fmb.12.74</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(1). Capsule presence is also associated with biofilm formation and allows colonisation of better survival as the thick capsule is hard to remove with detergents and other agents ADDIN EN.CITE <EndNote><Cite><Author>Huang</Author><Year>2014</Year><RecNum>35</RecNum><DisplayText>(6)</DisplayText><record><rec-number>35</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536543454″>35</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Huang, Tzu-Wen</author><author>Lam, Irene</author><author>Chang, Hwan-You</author><author>Tsai, Shih-Feng</author><author>Palsson, Bernhard O.</author><author>Charusanti, Pep</author></authors></contributors><titles><title>Capsule deletion via a ?-Red knockout system perturbs biofilm formation and fimbriae expression in Klebsiella pneumoniae MGH 78578</title><secondary-title>BMC Research Notes</secondary-title></titles><periodical><full-title>BMC Research Notes</full-title></periodical><pages>13-13</pages><volume>7</volume><dates><year>2014</year><pub-dates><date>01/08 08/01/received 12/31/accepted</date></pub-dates></dates><publisher>BioMed Central</publisher><isbn>1756-0500</isbn><accession-num>PMC3892127</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3892127/</url></related-urls></urls><electronic-resource-num>10.1186/1756-0500-7-13</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2).

0For Klebsiella pneumoniae formation of a biofilm allows for infection to occur through routes such as catheters and other medical instruments ADDIN EN.CITE <EndNote><Cite><Author>Murphy</Author><Year>2012</Year><RecNum>34</RecNum><DisplayText>(7)</DisplayText><record><rec-number>34</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536542638″>34</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Murphy, C. N.</author><author>Clegg, S.</author></authors></contributors><auth-address>Department of Microbiology, University of Iowa College of Medicine, Iowa City, IA 52242, USA.</auth-address><titles><title>Klebsiella pneumoniae and type 3 fimbriae: nosocomial infection, regulation and biofilm formation</title><secondary-title>Future Microbiol</secondary-title><alt-title>Future microbiology</alt-title></titles><periodical><full-title>Future Microbiol</full-title><abbr-1>Future microbiology</abbr-1></periodical><alt-periodical><full-title>Future Microbiol</full-title><abbr-1>Future microbiology</abbr-1></alt-periodical><pages>991-1002</pages><volume>7</volume><number>8</number><edition>2012/08/24</edition><keywords><keyword>Biofilms/*growth &amp; development</keyword><keyword>Catheter-Related Infections</keyword><keyword>Community-Acquired Infections/microbiology</keyword><keyword>Cross Infection/*microbiology</keyword><keyword>Cyclic GMP/analogs &amp; derivatives/metabolism</keyword><keyword>Fimbriae, Bacterial/*metabolism</keyword><keyword>Gene Expression Regulation, Bacterial</keyword><keyword>Humans</keyword><keyword>Klebsiella Infections/*microbiology</keyword><keyword>Klebsiella pneumoniae/*pathogenicity/*physiology</keyword><keyword>Virulence Factors/metabolism</keyword></keywords><dates><year>2012</year><pub-dates><date>Aug</date></pub-dates></dates><isbn>1746-0913</isbn><accession-num>22913357</accession-num><urls></urls><electronic-resource-num>10.2217/fmb.12.74</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(1). Catheters with a biofilm on them are one of the largest causes of nosocomial infections, as bacteria can evade host defence mechanisms and isn’t flushed out when urination occurs ADDIN EN.CITE <EndNote><Cite><Author>Murphy</Author><Year>2012</Year><RecNum>34</RecNum><DisplayText>(7)</DisplayText><record><rec-number>34</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536542638″>34</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Murphy, C. N.</author><author>Clegg, S.</author></authors></contributors><auth-address>Department of Microbiology, University of Iowa College of Medicine, Iowa City, IA 52242, USA.</auth-address><titles><title>Klebsiella pneumoniae and type 3 fimbriae: nosocomial infection, regulation and biofilm formation</title><secondary-title>Future Microbiol</secondary-title><alt-title>Future microbiology</alt-title></titles><periodical><full-title>Future Microbiol</full-title><abbr-1>Future microbiology</abbr-1></periodical><alt-periodical><full-title>Future Microbiol</full-title><abbr-1>Future microbiology</abbr-1></alt-periodical><pages>991-1002</pages><volume>7</volume><number>8</number><edition>2012/08/24</edition><keywords><keyword>Biofilms/*growth &amp; development</keyword><keyword>Catheter-Related Infections</keyword><keyword>Community-Acquired Infections/microbiology</keyword><keyword>Cross Infection/*microbiology</keyword><keyword>Cyclic GMP/analogs &amp; derivatives/metabolism</keyword><keyword>Fimbriae, Bacterial/*metabolism</keyword><keyword>Gene Expression Regulation, Bacterial</keyword><keyword>Humans</keyword><keyword>Klebsiella Infections/*microbiology</keyword><keyword>Klebsiella pneumoniae/*pathogenicity/*physiology</keyword><keyword>Virulence Factors/metabolism</keyword></keywords><dates><year>2012</year><pub-dates><date>Aug</date></pub-dates></dates><isbn>1746-0913</isbn><accession-num>22913357</accession-num><urls></urls><electronic-resource-num>10.2217/fmb.12.74</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(1). The surface expression of type 3 fimbriae in K. pneumoniae is an indicator of biofilm formation abilities, as these appendages mediate the initiation and colonisation and growth of biofilms ADDIN EN.CITE <EndNote><Cite><Author>Murphy</Author><Year>2012</Year><RecNum>34</RecNum><DisplayText>(7)</DisplayText><record><rec-number>34</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536542638″>34</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Murphy, C. N.</author><author>Clegg, S.</author></authors></contributors><auth-address>Department of Microbiology, University of Iowa College of Medicine, Iowa City, IA 52242, USA.</auth-address><titles><title>Klebsiella pneumoniae and type 3 fimbriae: nosocomial infection, regulation and biofilm formation</title><secondary-title>Future Microbiol</secondary-title><alt-title>Future microbiology</alt-title></titles><periodical><full-title>Future Microbiol</full-title><abbr-1>Future microbiology</abbr-1></periodical><alt-periodical><full-title>Future Microbiol</full-title><abbr-1>Future microbiology</abbr-1></alt-periodical><pages>991-1002</pages><volume>7</volume><number>8</number><edition>2012/08/24</edition><keywords><keyword>Biofilms/*growth &amp; development</keyword><keyword>Catheter-Related Infections</keyword><keyword>Community-Acquired Infections/microbiology</keyword><keyword>Cross Infection/*microbiology</keyword><keyword>Cyclic GMP/analogs &amp; derivatives/metabolism</keyword><keyword>Fimbriae, Bacterial/*metabolism</keyword><keyword>Gene Expression Regulation, Bacterial</keyword><keyword>Humans</keyword><keyword>Klebsiella Infections/*microbiology</keyword><keyword>Klebsiella pneumoniae/*pathogenicity/*physiology</keyword><keyword>Virulence Factors/metabolism</keyword></keywords><dates><year>2012</year><pub-dates><date>Aug</date></pub-dates></dates><isbn>1746-0913</isbn><accession-num>22913357</accession-num><urls></urls><electronic-resource-num>10.2217/fmb.12.74</electronic-resource-num><remote-database-provider>NLM</remote-database-provider><language>eng</language></record></Cite></EndNote>(1). Capsule presence is also associated with biofilm formation and allows colonisation of better survival as the thick capsule is hard to remove with detergents and other agents ADDIN EN.CITE <EndNote><Cite><Author>Huang</Author><Year>2014</Year><RecNum>35</RecNum><DisplayText>(6)</DisplayText><record><rec-number>35</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536543454″>35</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Huang, Tzu-Wen</author><author>Lam, Irene</author><author>Chang, Hwan-You</author><author>Tsai, Shih-Feng</author><author>Palsson, Bernhard O.</author><author>Charusanti, Pep</author></authors></contributors><titles><title>Capsule deletion via a ?-Red knockout system perturbs biofilm formation and fimbriae expression in Klebsiella pneumoniae MGH 78578</title><secondary-title>BMC Research Notes</secondary-title></titles><periodical><full-title>BMC Research Notes</full-title></periodical><pages>13-13</pages><volume>7</volume><dates><year>2014</year><pub-dates><date>01/08 08/01/received 12/31/accepted</date></pub-dates></dates><publisher>BioMed Central</publisher><isbn>1756-0500</isbn><accession-num>PMC3892127</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3892127/</url></related-urls></urls><electronic-resource-num>10.1186/1756-0500-7-13</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2).

QUESTION 1: Describe two important factors essential for biofilm development in K. pneumoniae, and how these factors are relevant to clinical settings.

-115083371564Klebsiella pneumoniae carbapenemase-producing (KPC) bacteria are often misidentified in standard susceptibility testing ADDIN EN.CITE <EndNote><Cite><Author>Arnold</Author><Year>2011</Year><RecNum>33</RecNum><DisplayText>(3)</DisplayText><record><rec-number>33</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536531078″>33</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Arnold, Ryan S.</author><author>Thom, Kerri A.</author><author>Sharma, Saarika</author><author>Phillips, Michael</author><author>Johnson, J. Kristie</author><author>Morgan, Daniel J.</author></authors></contributors><titles><title>Emergence of Klebsiella pneumoniae Carbapenemase (KPC)-Producing Bacteria</title><secondary-title>Southern medical journal</secondary-title></titles><periodical><full-title>Southern medical journal</full-title></periodical><pages>40-45</pages><volume>104</volume><number>1</number><dates><year>2011</year></dates><isbn>0038-4348 1541-8243</isbn><accession-num>PMC3075864</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075864/</url></related-urls></urls><electronic-resource-num>10.1097/SMJ.0b013e3181fd7d5a</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(3). They are frequently thought to be sensitive to carbapenem antibiotic when in fact they are resistant ADDIN EN.CITE <EndNote><Cite><Author>Arnold</Author><Year>2011</Year><RecNum>33</RecNum><DisplayText>(3)</DisplayText><record><rec-number>33</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536531078″>33</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Arnold, Ryan S.</author><author>Thom, Kerri A.</author><author>Sharma, Saarika</author><author>Phillips, Michael</author><author>Johnson, J. Kristie</author><author>Morgan, Daniel J.</author></authors></contributors><titles><title>Emergence of Klebsiella pneumoniae Carbapenemase (KPC)-Producing Bacteria</title><secondary-title>Southern medical journal</secondary-title></titles><periodical><full-title>Southern medical journal</full-title></periodical><pages>40-45</pages><volume>104</volume><number>1</number><dates><year>2011</year></dates><isbn>0038-4348 1541-8243</isbn><accession-num>PMC3075864</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075864/</url></related-urls></urls><electronic-resource-num>10.1097/SMJ.0b013e3181fd7d5a</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(3). In order to correctly diagnose KPC a ertapenem resistance test should be undertaken, as it gives indication of suspected KPC bacteria ADDIN EN.CITE <EndNote><Cite><Author>Arnold</Author><Year>2011</Year><RecNum>33</RecNum><DisplayText>(3)</DisplayText><record><rec-number>33</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536531078″>33</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Arnold, Ryan S.</author><author>Thom, Kerri A.</author><author>Sharma, Saarika</author><author>Phillips, Michael</author><author>Johnson, J. Kristie</author><author>Morgan, Daniel J.</author></authors></contributors><titles><title>Emergence of Klebsiella pneumoniae Carbapenemase (KPC)-Producing Bacteria</title><secondary-title>Southern medical journal</secondary-title></titles><periodical><full-title>Southern medical journal</full-title></periodical><pages>40-45</pages><volume>104</volume><number>1</number><dates><year>2011</year></dates><isbn>0038-4348 1541-8243</isbn><accession-num>PMC3075864</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075864/</url></related-urls></urls><electronic-resource-num>10.1097/SMJ.0b013e3181fd7d5a</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(3). KPC strains resistance works similarly to that of ESBL strains but the main issue is that carbapenem antibiotics are considered the in the medical industry as the ‘last resort’ antibiotic. This is a concern because there will be no way to fight bacteria that are resistance to carbapenem antibiotics.
0Klebsiella pneumoniae carbapenemase-producing (KPC) bacteria are often misidentified in standard susceptibility testing ADDIN EN.CITE <EndNote><Cite><Author>Arnold</Author><Year>2011</Year><RecNum>33</RecNum><DisplayText>(3)</DisplayText><record><rec-number>33</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536531078″>33</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Arnold, Ryan S.</author><author>Thom, Kerri A.</author><author>Sharma, Saarika</author><author>Phillips, Michael</author><author>Johnson, J. Kristie</author><author>Morgan, Daniel J.</author></authors></contributors><titles><title>Emergence of Klebsiella pneumoniae Carbapenemase (KPC)-Producing Bacteria</title><secondary-title>Southern medical journal</secondary-title></titles><periodical><full-title>Southern medical journal</full-title></periodical><pages>40-45</pages><volume>104</volume><number>1</number><dates><year>2011</year></dates><isbn>0038-4348 1541-8243</isbn><accession-num>PMC3075864</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075864/</url></related-urls></urls><electronic-resource-num>10.1097/SMJ.0b013e3181fd7d5a</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(3). They are frequently thought to be sensitive to carbapenem antibiotic when in fact they are resistant ADDIN EN.CITE <EndNote><Cite><Author>Arnold</Author><Year>2011</Year><RecNum>33</RecNum><DisplayText>(3)</DisplayText><record><rec-number>33</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536531078″>33</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Arnold, Ryan S.</author><author>Thom, Kerri A.</author><author>Sharma, Saarika</author><author>Phillips, Michael</author><author>Johnson, J. Kristie</author><author>Morgan, Daniel J.</author></authors></contributors><titles><title>Emergence of Klebsiella pneumoniae Carbapenemase (KPC)-Producing Bacteria</title><secondary-title>Southern medical journal</secondary-title></titles><periodical><full-title>Southern medical journal</full-title></periodical><pages>40-45</pages><volume>104</volume><number>1</number><dates><year>2011</year></dates><isbn>0038-4348 1541-8243</isbn><accession-num>PMC3075864</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075864/</url></related-urls></urls><electronic-resource-num>10.1097/SMJ.0b013e3181fd7d5a</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(3). In order to correctly diagnose KPC a ertapenem resistance test should be undertaken, as it gives indication of suspected KPC bacteria ADDIN EN.CITE <EndNote><Cite><Author>Arnold</Author><Year>2011</Year><RecNum>33</RecNum><DisplayText>(3)</DisplayText><record><rec-number>33</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536531078″>33</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Arnold, Ryan S.</author><author>Thom, Kerri A.</author><author>Sharma, Saarika</author><author>Phillips, Michael</author><author>Johnson, J. Kristie</author><author>Morgan, Daniel J.</author></authors></contributors><titles><title>Emergence of Klebsiella pneumoniae Carbapenemase (KPC)-Producing Bacteria</title><secondary-title>Southern medical journal</secondary-title></titles><periodical><full-title>Southern medical journal</full-title></periodical><pages>40-45</pages><volume>104</volume><number>1</number><dates><year>2011</year></dates><isbn>0038-4348 1541-8243</isbn><accession-num>PMC3075864</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075864/</url></related-urls></urls><electronic-resource-num>10.1097/SMJ.0b013e3181fd7d5a</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(3). KPC strains resistance works similarly to that of ESBL strains but the main issue is that carbapenem antibiotics are considered the in the medical industry as the ‘last resort’ antibiotic. This is a concern because there will be no way to fight bacteria that are resistance to carbapenem antibiotics.
QUESTION 2: Following identification of K. pneumoniae, the head physician predicted that the outbreak was caused by a KPC producing strain. What is KPC and how do KPC strains differ from ESBL strains?
QUESTION 3: Describe how the capsule may be regulated in K. pneumoniae to achieve a hypervirulent state.

-12571569126The thick, hypermucoviscous, extracellular polysaccharide capsule that surround K. pneumoniae is thought to be one of the major reasons for its high virulence ADDIN EN.CITE <EndNote><Cite><Author>Huang</Author><Year>2014</Year><RecNum>35</RecNum><DisplayText>(6)</DisplayText><record><rec-number>35</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536543454″>35</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Huang, Tzu-Wen</author><author>Lam, Irene</author><author>Chang, Hwan-You</author><author>Tsai, Shih-Feng</author><author>Palsson, Bernhard O.</author><author>Charusanti, Pep</author></authors></contributors><titles><title>Capsule deletion via a ?-Red knockout system perturbs biofilm formation and fimbriae expression in Klebsiella pneumoniae MGH 78578</title><secondary-title>BMC Research Notes</secondary-title></titles><periodical><full-title>BMC Research Notes</full-title></periodical><pages>13-13</pages><volume>7</volume><dates><year>2014</year><pub-dates><date>01/08 08/01/received 12/31/accepted</date></pub-dates></dates><publisher>BioMed Central</publisher><isbn>1756-0500</isbn><accession-num>PMC3892127</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3892127/</url></related-urls></urls><electronic-resource-num>10.1186/1756-0500-7-13</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). The capsule is a protective barrier for the bacteria and it protects it from phagocytosis, allowing the bacteria to survive in the body much longer ADDIN EN.CITE <EndNote><Cite><Author>Huang</Author><Year>2014</Year><RecNum>35</RecNum><DisplayText>(6)</DisplayText><record><rec-number>35</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536543454″>35</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Huang, Tzu-Wen</author><author>Lam, Irene</author><author>Chang, Hwan-You</author><author>Tsai, Shih-Feng</author><author>Palsson, Bernhard O.</author><author>Charusanti, Pep</author></authors></contributors><titles><title>Capsule deletion via a ?-Red knockout system perturbs biofilm formation and fimbriae expression in Klebsiella pneumoniae MGH 78578</title><secondary-title>BMC Research Notes</secondary-title></titles><periodical><full-title>BMC Research Notes</full-title></periodical><pages>13-13</pages><volume>7</volume><dates><year>2014</year><pub-dates><date>01/08 08/01/received 12/31/accepted</date></pub-dates></dates><publisher>BioMed Central</publisher><isbn>1756-0500</isbn><accession-num>PMC3892127</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3892127/</url></related-urls></urls><electronic-resource-num>10.1186/1756-0500-7-13</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). The hypervirulent state is often associated with an overproduction of the capsular polysaccharide which is mediated by the gene magA, rmpA and rmpA2 ADDIN EN.CITE <EndNote><Cite><Author>Dorman</Author><Year>2018</Year><RecNum>36</RecNum><DisplayText>(10)</DisplayText><record><rec-number>36</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536544412″>36</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Dorman, Matthew J.</author><author>Feltwell, Theresa</author><author>Goulding, David</author><author>Parkhill, Julian</author><author>Short, Francesca L.</author></authors></contributors><titles><title>The capsule regulatory network of Klebsiella pneumoniae defined by density-TraDISort</title><secondary-title>bioRxiv</secondary-title></titles><periodical><full-title>bioRxiv</full-title></periodical><dates><year>2018</year></dates><work-type>10.1101/404400</work-type><urls><related-urls><url>http://biorxiv.org/content/early/2018/08/31/404400.abstract</url></related-urls></urls></record></Cite></EndNote>(4). All these genes effect the mucoviscosity and positively regulate capsule synthesis ADDIN EN.CITE <EndNote><Cite><Author>Dorman</Author><Year>2018</Year><RecNum>36</RecNum><DisplayText>(10)</DisplayText><record><rec-number>36</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536544412″>36</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Dorman, Matthew J.</author><author>Feltwell, Theresa</author><author>Goulding, David</author><author>Parkhill, Julian</author><author>Short, Francesca L.</author></authors></contributors><titles><title>The capsule regulatory network of Klebsiella pneumoniae defined by density-TraDISort</title><secondary-title>bioRxiv</secondary-title></titles><periodical><full-title>bioRxiv</full-title></periodical><dates><year>2018</year></dates><work-type>10.1101/404400</work-type><urls><related-urls><url>http://biorxiv.org/content/early/2018/08/31/404400.abstract</url></related-urls></urls></record></Cite></EndNote>(4).
0The thick, hypermucoviscous, extracellular polysaccharide capsule that surround K. pneumoniae is thought to be one of the major reasons for its high virulence ADDIN EN.CITE <EndNote><Cite><Author>Huang</Author><Year>2014</Year><RecNum>35</RecNum><DisplayText>(6)</DisplayText><record><rec-number>35</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536543454″>35</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Huang, Tzu-Wen</author><author>Lam, Irene</author><author>Chang, Hwan-You</author><author>Tsai, Shih-Feng</author><author>Palsson, Bernhard O.</author><author>Charusanti, Pep</author></authors></contributors><titles><title>Capsule deletion via a ?-Red knockout system perturbs biofilm formation and fimbriae expression in Klebsiella pneumoniae MGH 78578</title><secondary-title>BMC Research Notes</secondary-title></titles><periodical><full-title>BMC Research Notes</full-title></periodical><pages>13-13</pages><volume>7</volume><dates><year>2014</year><pub-dates><date>01/08 08/01/received 12/31/accepted</date></pub-dates></dates><publisher>BioMed Central</publisher><isbn>1756-0500</isbn><accession-num>PMC3892127</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3892127/</url></related-urls></urls><electronic-resource-num>10.1186/1756-0500-7-13</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). The capsule is a protective barrier for the bacteria and it protects it from phagocytosis, allowing the bacteria to survive in the body much longer ADDIN EN.CITE <EndNote><Cite><Author>Huang</Author><Year>2014</Year><RecNum>35</RecNum><DisplayText>(6)</DisplayText><record><rec-number>35</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536543454″>35</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Huang, Tzu-Wen</author><author>Lam, Irene</author><author>Chang, Hwan-You</author><author>Tsai, Shih-Feng</author><author>Palsson, Bernhard O.</author><author>Charusanti, Pep</author></authors></contributors><titles><title>Capsule deletion via a ?-Red knockout system perturbs biofilm formation and fimbriae expression in Klebsiella pneumoniae MGH 78578</title><secondary-title>BMC Research Notes</secondary-title></titles><periodical><full-title>BMC Research Notes</full-title></periodical><pages>13-13</pages><volume>7</volume><dates><year>2014</year><pub-dates><date>01/08 08/01/received 12/31/accepted</date></pub-dates></dates><publisher>BioMed Central</publisher><isbn>1756-0500</isbn><accession-num>PMC3892127</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3892127/</url></related-urls></urls><electronic-resource-num>10.1186/1756-0500-7-13</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). The hypervirulent state is often associated with an overproduction of the capsular polysaccharide which is mediated by the gene magA, rmpA and rmpA2 ADDIN EN.CITE <EndNote><Cite><Author>Dorman</Author><Year>2018</Year><RecNum>36</RecNum><DisplayText>(10)</DisplayText><record><rec-number>36</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536544412″>36</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Dorman, Matthew J.</author><author>Feltwell, Theresa</author><author>Goulding, David</author><author>Parkhill, Julian</author><author>Short, Francesca L.</author></authors></contributors><titles><title>The capsule regulatory network of Klebsiella pneumoniae defined by density-TraDISort</title><secondary-title>bioRxiv</secondary-title></titles><periodical><full-title>bioRxiv</full-title></periodical><dates><year>2018</year></dates><work-type>10.1101/404400</work-type><urls><related-urls><url>http://biorxiv.org/content/early/2018/08/31/404400.abstract</url></related-urls></urls></record></Cite></EndNote>(4). All these genes effect the mucoviscosity and positively regulate capsule synthesis ADDIN EN.CITE <EndNote><Cite><Author>Dorman</Author><Year>2018</Year><RecNum>36</RecNum><DisplayText>(10)</DisplayText><record><rec-number>36</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536544412″>36</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Dorman, Matthew J.</author><author>Feltwell, Theresa</author><author>Goulding, David</author><author>Parkhill, Julian</author><author>Short, Francesca L.</author></authors></contributors><titles><title>The capsule regulatory network of Klebsiella pneumoniae defined by density-TraDISort</title><secondary-title>bioRxiv</secondary-title></titles><periodical><full-title>bioRxiv</full-title></periodical><dates><year>2018</year></dates><work-type>10.1101/404400</work-type><urls><related-urls><url>http://biorxiv.org/content/early/2018/08/31/404400.abstract</url></related-urls></urls></record></Cite></EndNote>(4).

References (1/4 page)
-115083707511 Murphy CN, Clegg S. Klebsiella pneumoniae and type 3 fimbriae: nosocomial infection, regulation and biofilm formation. Future microbiology. 2012;7(8):991-1002.

2Huang, T.-W., Lam, I., Chang, H.-Y., Tsai, S.-F., Palsson, B. O., & Charusanti, P. (2014). Capsule deletion via a ?-Red knockout system perturbs biofilm formation and fimbriae expression in Klebsiella pneumoniae MGH 78578. BMC Research Notes, 7, 13-13. doi:10.1186/1756-0500-7-13
3Arnold, R. S., Thom, K. A., Sharma, S., Phillips, M., Johnson, J. K., & Morgan, D. J. (2011). Emergence of Klebsiella pneumoniae Carbapenemase (KPC)-Producing Bacteria. Southern medical journal, 104(1), 40-45. doi:10.1097/SMJ.0b013e3181fd7d5a
4Dorman, M. J., Feltwell, T., Goulding, D., Parkhill, J., & Short, F. L. (2018). The capsule regulatory network of Klebsiella pneumoniae defined by density-TraDISort. bioRxiv.
01 Murphy CN, Clegg S. Klebsiella pneumoniae and type 3 fimbriae: nosocomial infection, regulation and biofilm formation. Future microbiology. 2012;7(8):991-1002.

2Huang, T.-W., Lam, I., Chang, H.-Y., Tsai, S.-F., Palsson, B. O., & Charusanti, P. (2014). Capsule deletion via a ?-Red knockout system perturbs biofilm formation and fimbriae expression in Klebsiella pneumoniae MGH 78578. BMC Research Notes, 7, 13-13. doi:10.1186/1756-0500-7-13
3Arnold, R. S., Thom, K. A., Sharma, S., Phillips, M., Johnson, J. K., & Morgan, D. J. (2011). Emergence of Klebsiella pneumoniae Carbapenemase (KPC)-Producing Bacteria. Southern medical journal, 104(1), 40-45. doi:10.1097/SMJ.0b013e3181fd7d5a
4Dorman, M. J., Feltwell, T., Goulding, D., Parkhill, J., & Short, F. L. (2018). The capsule regulatory network of Klebsiella pneumoniae defined by density-TraDISort. bioRxiv.

Module 1: Bacterial Pathogenesis
Laboratory report 3
A. BAUMANNII CLONAL TYPING (Part A) weekS 5-6
and GENE REGULATION (Part B) week 6
-121285191771To examine the global spread of the A. baumannii GC2 clonal lineage to allow the tracing of the antibiotic resistance genes associated.
0To examine the global spread of the A. baumannii GC2 clonal lineage to allow the tracing of the antibiotic resistance genes associated.
What was the aim of your investigation? (1-2 sentences)
-125715192347A MLST analysis of different A. baumannii isolates was conducted. This test was conducted to determine the differences in strains of the bacteria and trace the bacterial resistance. Using forward and reverse primers to isolate the targeted allele, the analysis was conducted using a PCR cycle. The primers used for an MLST analysis target seven housekeeping genes within A. baumanni. The PCR cycle was used to amplify the housekeeping genes and this was checked by running a gel, which was visualised using a UV trans-illuminator. An online comparison of antibiotic resistance islands was also conducted and a phylogenic tree was obtained. In the GC2 lineage of A. baumannii, resistance genes are commonly found on A. baumannii genomic resistance islands (AbGRIs). To compare and contrast the differences in the GC2 strain, the multiple sequence alignment and phylogenic tree were generated. These documents allowed for comparison of the genes at ABGRI3 to be compared within the GC2 clonal group. A test was undertaken to measure the activity of Beta-galactosidase enzyme from cultures grown in the presence of glucose, lactose or both. This was determined by using ONPG solution which is hydrolysed by beta-galactosidase and produces a yellow colour. This was determined by inoculating sterile saline with the cultures, adding chloroform to liberate the enzyme and ONPG solution. The tubes were incubated at 37°C for up to 4 hours. Results were read at the 2-hour mark with a colour change to yellow being a positive result. This tests is used to allow analysis of bacterial gene regulation.
0A MLST analysis of different A. baumannii isolates was conducted. This test was conducted to determine the differences in strains of the bacteria and trace the bacterial resistance. Using forward and reverse primers to isolate the targeted allele, the analysis was conducted using a PCR cycle. The primers used for an MLST analysis target seven housekeeping genes within A. baumanni. The PCR cycle was used to amplify the housekeeping genes and this was checked by running a gel, which was visualised using a UV trans-illuminator. An online comparison of antibiotic resistance islands was also conducted and a phylogenic tree was obtained. In the GC2 lineage of A. baumannii, resistance genes are commonly found on A. baumannii genomic resistance islands (AbGRIs). To compare and contrast the differences in the GC2 strain, the multiple sequence alignment and phylogenic tree were generated. These documents allowed for comparison of the genes at ABGRI3 to be compared within the GC2 clonal group. A test was undertaken to measure the activity of Beta-galactosidase enzyme from cultures grown in the presence of glucose, lactose or both. This was determined by using ONPG solution which is hydrolysed by beta-galactosidase and produces a yellow colour. This was determined by inoculating sterile saline with the cultures, adding chloroform to liberate the enzyme and ONPG solution. The tubes were incubated at 37°C for up to 4 hours. Results were read at the 2-hour mark with a colour change to yellow being a positive result. This tests is used to allow analysis of bacterial gene regulation.
Briefly summarise the methods and describe their purpose in addressing the aim(1/4 page)
Report your results and findings. (1/2 – 1 page)
-123696114556Table 1: ONPG ?-galactosidase test which is indicated by a colour change in a E.coli solution in the presence of ONPG and ?-galactosidase
Sample Result
Glucose Negative- clear
Lactose Positive- darker
Glucose and Lactose Positive-lighter
Table 2: Sequence analysis of alleles using the MLST database to determine allele numbers and sequence types
ALLELE NUMBER ABXH3 3070294 6200 BH1AB SGH0908 TYTH1
cpn60 2 1 5 1 1 2
fusA2 1 2 2 2 2
gltA2 1 4 2 2 2
pyrG2 1 1 2 2 2
recA2 1 3 2 2 2
rplB2 1 4 2 2 2
rpoB2 1 4 2 2 2
SEQUENCE TYPE 2 8 464 98 98 2

Figure SEQ Figure * ARABIC 1- Phylogenic tree showing the relationship between the genome AbGR13 and its differing strains. The above phylogenic tree indicates that there is one allele different between the different strains of the AbGR13 genome.
0Table 1: ONPG ?-galactosidase test which is indicated by a colour change in a E.coli solution in the presence of ONPG and ?-galactosidase
Sample Result
Glucose Negative- clear
Lactose Positive- darker
Glucose and Lactose Positive-lighter
Table 2: Sequence analysis of alleles using the MLST database to determine allele numbers and sequence types
ALLELE NUMBER ABXH3 3070294 6200 BH1AB SGH0908 TYTH1
cpn60 2 1 5 1 1 2
fusA2 1 2 2 2 2
gltA2 1 4 2 2 2
pyrG2 1 1 2 2 2
recA2 1 3 2 2 2
rplB2 1 4 2 2 2
rpoB2 1 4 2 2 2
SEQUENCE TYPE 2 8 464 98 98 2

Figure SEQ Figure * ARABIC 1- Phylogenic tree showing the relationship between the genome AbGR13 and its differing strains. The above phylogenic tree indicates that there is one allele different between the different strains of the AbGR13 genome.

Conclusions (2-3 sentences)
-7865841671Two of the samples examined have the same sequence types (ABXH3 and TYTH1, BH1AB and SGH0908) when considering the housekeeping genes analysed using MLST. This indicates that whilst the strains come from geographically different areas, they share common ancestors. The E.coli experiment showed how the lac operon is turned on and off depending on what the bacteria has at its disposal for cellular functions.
0Two of the samples examined have the same sequence types (ABXH3 and TYTH1, BH1AB and SGH0908) when considering the housekeeping genes analysed using MLST. This indicates that whilst the strains come from geographically different areas, they share common ancestors. The E.coli experiment showed how the lac operon is turned on and off depending on what the bacteria has at its disposal for cellular functions.

Discussion of results in relation to pathogenesis. (3/4 page total; 2-4 sentences for each answer)
(this will be based on independent or laboratory/workshop-directed research you have performed)
-123696401545One major disadvantage of using MLST to track a pathogen is that it only uses seven loci in its detection. These seven loci are all core housekeeping genes, which are then compared using a database to determine polymorphisms. This is a limitation as the genes that influence the pathogen may be in elsewhere and therefore not detected. As no genes other than these housekeeping genes are being investigated for polymorphisms there isn’t a full picture being determined.
0One major disadvantage of using MLST to track a pathogen is that it only uses seven loci in its detection. These seven loci are all core housekeeping genes, which are then compared using a database to determine polymorphisms. This is a limitation as the genes that influence the pathogen may be in elsewhere and therefore not detected. As no genes other than these housekeeping genes are being investigated for polymorphisms there isn’t a full picture being determined.
QUESTION 1: Explain one disadvantage of using MLST as a method of tracking pathogens that was demonstrated in this learning module.

-123696209727The lac operon is a bundle of genes that cells require to produce the enzymes to process lactose ADDIN EN.CITE <EndNote><Cite><Author>Aguda</Author><Year>2008</Year><RecNum>28</RecNum><DisplayText>(1)</DisplayText><record><rec-number>28</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1535925235″>28</key></foreign-keys><ref-type name=”Book”>6</ref-type><contributors><authors><author>Aguda, B.</author><author>Friedman, A.</author><author>Oxford University Press</author></authors></contributors><titles><title>Models of Cellular Regulation</title></titles><section>52-54</section><dates><year>2008</year></dates><publisher>OUP Oxford</publisher><isbn>9780198570912</isbn><urls><related-urls><url>https://books.google.com.au/books?id=_y4TDAAAQBAJ</url></related-urls></urls></record></Cite></EndNote>(1). As glucose is the preferred energy source for most, if not all, bacteria this operon is only switched on in the absence of glucose and presence of lactose ADDIN EN.CITE <EndNote><Cite><Author>Aguda</Author><Year>2008</Year><RecNum>28</RecNum><DisplayText>(1)</DisplayText><record><rec-number>28</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1535925235″>28</key></foreign-keys><ref-type name=”Book”>6</ref-type><contributors><authors><author>Aguda, B.</author><author>Friedman, A.</author><author>Oxford University Press</author></authors></contributors><titles><title>Models of Cellular Regulation</title></titles><section>52-54</section><dates><year>2008</year></dates><publisher>OUP Oxford</publisher><isbn>9780198570912</isbn><urls><related-urls><url>https://books.google.com.au/books?id=_y4TDAAAQBAJ</url></related-urls></urls></record></Cite></EndNote>(1). The bacteria brings external lactose into the cell when the lac operon is switched on, which is then metabolised by the cell ADDIN EN.CITE <EndNote><Cite><Author>Aguda</Author><Year>2008</Year><RecNum>28</RecNum><DisplayText>(1)</DisplayText><record><rec-number>28</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1535925235″>28</key></foreign-keys><ref-type name=”Book”>6</ref-type><contributors><authors><author>Aguda, B.</author><author>Friedman, A.</author><author>Oxford University Press</author></authors></contributors><titles><title>Models of Cellular Regulation</title></titles><section>52-54</section><dates><year>2008</year></dates><publisher>OUP Oxford</publisher><isbn>9780198570912</isbn><urls><related-urls><url>https://books.google.com.au/books?id=_y4TDAAAQBAJ</url></related-urls></urls></record></Cite></EndNote>(1). As lactose is the sugar that switches on the lac operon, it is known as the inducer.
0The lac operon is a bundle of genes that cells require to produce the enzymes to process lactose ADDIN EN.CITE <EndNote><Cite><Author>Aguda</Author><Year>2008</Year><RecNum>28</RecNum><DisplayText>(1)</DisplayText><record><rec-number>28</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1535925235″>28</key></foreign-keys><ref-type name=”Book”>6</ref-type><contributors><authors><author>Aguda, B.</author><author>Friedman, A.</author><author>Oxford University Press</author></authors></contributors><titles><title>Models of Cellular Regulation</title></titles><section>52-54</section><dates><year>2008</year></dates><publisher>OUP Oxford</publisher><isbn>9780198570912</isbn><urls><related-urls><url>https://books.google.com.au/books?id=_y4TDAAAQBAJ</url></related-urls></urls></record></Cite></EndNote>(1). As glucose is the preferred energy source for most, if not all, bacteria this operon is only switched on in the absence of glucose and presence of lactose ADDIN EN.CITE <EndNote><Cite><Author>Aguda</Author><Year>2008</Year><RecNum>28</RecNum><DisplayText>(1)</DisplayText><record><rec-number>28</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1535925235″>28</key></foreign-keys><ref-type name=”Book”>6</ref-type><contributors><authors><author>Aguda, B.</author><author>Friedman, A.</author><author>Oxford University Press</author></authors></contributors><titles><title>Models of Cellular Regulation</title></titles><section>52-54</section><dates><year>2008</year></dates><publisher>OUP Oxford</publisher><isbn>9780198570912</isbn><urls><related-urls><url>https://books.google.com.au/books?id=_y4TDAAAQBAJ</url></related-urls></urls></record></Cite></EndNote>(1). The bacteria brings external lactose into the cell when the lac operon is switched on, which is then metabolised by the cell ADDIN EN.CITE <EndNote><Cite><Author>Aguda</Author><Year>2008</Year><RecNum>28</RecNum><DisplayText>(1)</DisplayText><record><rec-number>28</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1535925235″>28</key></foreign-keys><ref-type name=”Book”>6</ref-type><contributors><authors><author>Aguda, B.</author><author>Friedman, A.</author><author>Oxford University Press</author></authors></contributors><titles><title>Models of Cellular Regulation</title></titles><section>52-54</section><dates><year>2008</year></dates><publisher>OUP Oxford</publisher><isbn>9780198570912</isbn><urls><related-urls><url>https://books.google.com.au/books?id=_y4TDAAAQBAJ</url></related-urls></urls></record></Cite></EndNote>(1). As lactose is the sugar that switches on the lac operon, it is known as the inducer.
QUESTION 2: From your results, which sugar induces the lac operon? How does it achieve this?
QUESTION 3: Discuss how the regulation of genes can have an effect on the virulence potential of a bacterial pathogen. Use A. baumannii as an example to explain your answer.

-12571523244Regulation of gene expression can effect the virulence potential of bacteria’s through the up and down regulation of certain factors. In A. baumannii, the regulation of different two-component systems and the associated genes have multiple effects ADDIN EN.CITE <EndNote><Cite><Author>Kröger</Author><Year>2017</Year><RecNum>38</RecNum><DisplayText>(5)</DisplayText><record><rec-number>38</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536547381″>38</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Kröger, Carsten</author><author>Kary, Stefani C.</author><author>Schauer, Kristina</author><author>Cameron, Andrew D. S.</author></authors></contributors><titles><title>Genetic Regulation of Virulence and Antibiotic Resistance in Acinetobacter baumannii</title><secondary-title>Genes</secondary-title></titles><periodical><full-title>Genes</full-title></periodical><pages>12</pages><volume>8</volume><number>1</number><dates><year>2017</year><pub-dates><date>12/28 09/22/received 12/20/accepted</date></pub-dates></dates><publisher>MDPI</publisher><isbn>2073-4425</isbn><accession-num>PMC5295007</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295007/</url></related-urls></urls><electronic-resource-num>10.3390/genes8010012</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). The gene adeRS controls 579 other genes and regulates the expression of a drug efflux pump ADDIN EN.CITE <EndNote><Cite><Author>Kröger</Author><Year>2017</Year><RecNum>38</RecNum><DisplayText>(5)</DisplayText><record><rec-number>38</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536547381″>38</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Kröger, Carsten</author><author>Kary, Stefani C.</author><author>Schauer, Kristina</author><author>Cameron, Andrew D. S.</author></authors></contributors><titles><title>Genetic Regulation of Virulence and Antibiotic Resistance in Acinetobacter baumannii</title><secondary-title>Genes</secondary-title></titles><periodical><full-title>Genes</full-title></periodical><pages>12</pages><volume>8</volume><number>1</number><dates><year>2017</year><pub-dates><date>12/28 09/22/received 12/20/accepted</date></pub-dates></dates><publisher>MDPI</publisher><isbn>2073-4425</isbn><accession-num>PMC5295007</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295007/</url></related-urls></urls><electronic-resource-num>10.3390/genes8010012</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). This gene is also required for biofilm formation which increases the ability of this bacteria to cause infection ADDIN EN.CITE <EndNote><Cite><Author>Kröger</Author><Year>2017</Year><RecNum>38</RecNum><DisplayText>(5)</DisplayText><record><rec-number>38</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536547381″>38</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Kröger, Carsten</author><author>Kary, Stefani C.</author><author>Schauer, Kristina</author><author>Cameron, Andrew D. S.</author></authors></contributors><titles><title>Genetic Regulation of Virulence and Antibiotic Resistance in Acinetobacter baumannii</title><secondary-title>Genes</secondary-title></titles><periodical><full-title>Genes</full-title></periodical><pages>12</pages><volume>8</volume><number>1</number><dates><year>2017</year><pub-dates><date>12/28 09/22/received 12/20/accepted</date></pub-dates></dates><publisher>MDPI</publisher><isbn>2073-4425</isbn><accession-num>PMC5295007</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295007/</url></related-urls></urls><electronic-resource-num>10.3390/genes8010012</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). The gene pmrAB when upregulated in A. baumanni causes resistance to colistin, making the bacteria harder to kill ADDIN EN.CITE <EndNote><Cite><Author>Kröger</Author><Year>2017</Year><RecNum>38</RecNum><DisplayText>(5)</DisplayText><record><rec-number>38</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536547381″>38</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Kröger, Carsten</author><author>Kary, Stefani C.</author><author>Schauer, Kristina</author><author>Cameron, Andrew D. S.</author></authors></contributors><titles><title>Genetic Regulation of Virulence and Antibiotic Resistance in Acinetobacter baumannii</title><secondary-title>Genes</secondary-title></titles><periodical><full-title>Genes</full-title></periodical><pages>12</pages><volume>8</volume><number>1</number><dates><year>2017</year><pub-dates><date>12/28 09/22/received 12/20/accepted</date></pub-dates></dates><publisher>MDPI</publisher><isbn>2073-4425</isbn><accession-num>PMC5295007</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295007/</url></related-urls></urls><electronic-resource-num>10.3390/genes8010012</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). If multiple genes in the cell are regulated to increase virulence then the pathogen is more effective overall.
0Regulation of gene expression can effect the virulence potential of bacteria’s through the up and down regulation of certain factors. In A. baumannii, the regulation of different two-component systems and the associated genes have multiple effects ADDIN EN.CITE <EndNote><Cite><Author>Kröger</Author><Year>2017</Year><RecNum>38</RecNum><DisplayText>(5)</DisplayText><record><rec-number>38</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536547381″>38</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Kröger, Carsten</author><author>Kary, Stefani C.</author><author>Schauer, Kristina</author><author>Cameron, Andrew D. S.</author></authors></contributors><titles><title>Genetic Regulation of Virulence and Antibiotic Resistance in Acinetobacter baumannii</title><secondary-title>Genes</secondary-title></titles><periodical><full-title>Genes</full-title></periodical><pages>12</pages><volume>8</volume><number>1</number><dates><year>2017</year><pub-dates><date>12/28 09/22/received 12/20/accepted</date></pub-dates></dates><publisher>MDPI</publisher><isbn>2073-4425</isbn><accession-num>PMC5295007</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295007/</url></related-urls></urls><electronic-resource-num>10.3390/genes8010012</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). The gene adeRS controls 579 other genes and regulates the expression of a drug efflux pump ADDIN EN.CITE <EndNote><Cite><Author>Kröger</Author><Year>2017</Year><RecNum>38</RecNum><DisplayText>(5)</DisplayText><record><rec-number>38</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536547381″>38</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Kröger, Carsten</author><author>Kary, Stefani C.</author><author>Schauer, Kristina</author><author>Cameron, Andrew D. S.</author></authors></contributors><titles><title>Genetic Regulation of Virulence and Antibiotic Resistance in Acinetobacter baumannii</title><secondary-title>Genes</secondary-title></titles><periodical><full-title>Genes</full-title></periodical><pages>12</pages><volume>8</volume><number>1</number><dates><year>2017</year><pub-dates><date>12/28 09/22/received 12/20/accepted</date></pub-dates></dates><publisher>MDPI</publisher><isbn>2073-4425</isbn><accession-num>PMC5295007</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295007/</url></related-urls></urls><electronic-resource-num>10.3390/genes8010012</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). This gene is also required for biofilm formation which increases the ability of this bacteria to cause infection ADDIN EN.CITE <EndNote><Cite><Author>Kröger</Author><Year>2017</Year><RecNum>38</RecNum><DisplayText>(5)</DisplayText><record><rec-number>38</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536547381″>38</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Kröger, Carsten</author><author>Kary, Stefani C.</author><author>Schauer, Kristina</author><author>Cameron, Andrew D. S.</author></authors></contributors><titles><title>Genetic Regulation of Virulence and Antibiotic Resistance in Acinetobacter baumannii</title><secondary-title>Genes</secondary-title></titles><periodical><full-title>Genes</full-title></periodical><pages>12</pages><volume>8</volume><number>1</number><dates><year>2017</year><pub-dates><date>12/28 09/22/received 12/20/accepted</date></pub-dates></dates><publisher>MDPI</publisher><isbn>2073-4425</isbn><accession-num>PMC5295007</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295007/</url></related-urls></urls><electronic-resource-num>10.3390/genes8010012</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). The gene pmrAB when upregulated in A. baumanni causes resistance to colistin, making the bacteria harder to kill ADDIN EN.CITE <EndNote><Cite><Author>Kröger</Author><Year>2017</Year><RecNum>38</RecNum><DisplayText>(5)</DisplayText><record><rec-number>38</rec-number><foreign-keys><key app=”EN” db-id=”dpesz9ev2xwpt8exa5e52ssf2xt0fdszvxpx” timestamp=”1536547381″>38</key></foreign-keys><ref-type name=”Journal Article”>17</ref-type><contributors><authors><author>Kröger, Carsten</author><author>Kary, Stefani C.</author><author>Schauer, Kristina</author><author>Cameron, Andrew D. S.</author></authors></contributors><titles><title>Genetic Regulation of Virulence and Antibiotic Resistance in Acinetobacter baumannii</title><secondary-title>Genes</secondary-title></titles><periodical><full-title>Genes</full-title></periodical><pages>12</pages><volume>8</volume><number>1</number><dates><year>2017</year><pub-dates><date>12/28 09/22/received 12/20/accepted</date></pub-dates></dates><publisher>MDPI</publisher><isbn>2073-4425</isbn><accession-num>PMC5295007</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295007/</url></related-urls></urls><electronic-resource-num>10.3390/genes8010012</electronic-resource-num><remote-database-name>PMC</remote-database-name></record></Cite></EndNote>(2). If multiple genes in the cell are regulated to increase virulence then the pathogen is more effective overall.

-1095621783371 ADDIN EN.REFLIST Aguda, B., Friedman, A., & Press, O. U. (2008). Models of Cellular Regulation: OUP Oxford.

2Kröger, C., Kary, S. C., Schauer, K., & Cameron, A. D. S. (2017). Genetic Regulation of Virulence and Antibiotic Resistance in Acinetobacter baumannii. Genes, 8(1), 12. doi:10.3390/genes8010012
01 ADDIN EN.REFLIST Aguda, B., Friedman, A., & Press, O. U. (2008). Models of Cellular Regulation: OUP Oxford.

2Kröger, C., Kary, S. C., Schauer, K., & Cameron, A. D. S. (2017). Genetic Regulation of Virulence and Antibiotic Resistance in Acinetobacter baumannii. Genes, 8(1), 12. doi:10.3390/genes8010012
References (1/4 page)