The Escherichia coli bacteria produces an enzyme that can inactivate ẞ-lactam antibiotics. By contrast, the Salmonella enterica bacteria is killed by ẞ-lactam antibiotics. When a community contains both types of bacteria, fewer of the Salmonella enterica bacteria are killed. This is an example of Exposure protection Gene Mutation Protection mediated by interspecies communication Vulnerability due to cross feeding
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- In 2013, there was an outbreak of methicillin-resistant Staphylococcusaureus (MRSA) at an NFL training facility. One player suffereda career-ending infection to his foot and sued the team owners for $20 million for unsanitary conditions that contributed to the bacterialinfection. A settlement with undisclosed terms was reached in2017. MRSA is highly contagious and is spread by direct skin contactor by airborne transmission and can result in amputation or death.In addition, MRSA is very difficult to treat because it is resistant tomany antibiotics. For example, b -lactam antibiotics, such as penicillin,function by binding to and inactivating bacterial penicillin-bindingproteins (PBPs), which synthesize the bacterial cell wall. However,MRSA expresses an alternative type of PBP, called PBP2a encodedby the mecA gene. b -lactam antibiotics only weakly bind PBP2a,and thus cell wall synthesis can continue in their presence. Moreover,in a system somewhat analogous to the regulation of the…In 2013, there was an outbreak of methicillin-resistant Staphylococcusaureus (MRSA) at an NFL training facility. One player suffereda career-ending infection to his foot and sued the team owners for $20 million for unsanitary conditions that contributed to the bacterialinfection. A settlement with undisclosed terms was reached in2017. MRSA is highly contagious and is spread by direct skin contactor by airborne transmission and can result in amputation or death.In addition, MRSA is very difficult to treat because it is resistant tomany antibiotics. For example, b -lactam antibiotics, such as penicillin,function by binding to and inactivating bacterial penicillin-bindingproteins (PBPs), which synthesize the bacterial cell wall. However,MRSA expresses an alternative type of PBP, called PBP2a encodedby the mecA gene. b -lactam antibiotics only weakly bind PBP2a,and thus cell wall synthesis can continue in their presence. Moreover,in a system somewhat analogous to the regulation of the…Please answer the one question below, thanks In 2013, there was an outbreak of methicillin-resistant Staphylococcus aureus (MRSA) at an NFL training facility. One player suffered a career-ending infection to his foot and sued the team owners for $20 million for unsanitary conditions that contributed to the bacterial infection. A settlement with undisclosed terms was reached in 2017. MRSA is highly contagious and is spread by direct skin contact or by airborne transmission and can result in amputation or death. In addition, MRSA is very difficult to treat because it is resistant to many antibiotics. For example, β-lactamβ-lactam antibiotics, such as penicillin, function by binding to and inactivating bacterial penicillin-binding proteins (PBPs), which synthesize the bacterial cell wall. However, MRSA expresses an alternative type of PBP, called PBP2a encoded by the mecA gene. β-lactamβ-lactam antibiotics only weakly bind PBP2a, and thus cell wall synthesis can continue in their…
- The vaccine for Haemophilus influenzae type b is called a conjugate vaccine. It is composed of the tetanus toxoid protein conjugated to the capsular polysaccharide of the H. influenzae type b bacteria. When used to vaccinate infants, the antibody response generated by this vaccine would include 0 0 0 0 antibodies that bind only to the protein-polysaccharide conjugate in the vaccine. antibodies to the tetanus toxoid only. antibodies to the bacterial polysaccharide and the tetanus toxoid. antibodies to the bacterial polysaccharide only.Pathogens have a variety of traits that interact with a host and enable the pathogen to enter a host, adhere to host cells, gain access to nutrients, and escape detection or removal by the immune system. These traits are called virulence factors. The following enzymes and toxin can act as virulence factors and contribute to bacteria’s pathogenicity. What are the specific actions of the following enzymes and toxin that make them virulence factors? Coagulase Kinase (such as staphylokinases and streptokinases) Hyaluronidase Collagenase CytotoxinA white blood cell has pathogen recognition proteins embedded in its plasma membrane. Initially, the the pathogen recognition proteins are spread over the whole surface of the white blood cell. The white blood cell comes into contact with a bacterial cell. Some of the pathogen recognition proteins bind to the lipoteichoic acid molecules on the surface of the bacterial cell. As time goes on, more and more of the pathogen recognition proteins bind to the lipoteichoic acid molecules on the bacterial cell surface. The white blood cell membrane at the point of contact between these 2 cells now contains a dense cluster pathogen recognition proteins. How is it possible for the pathogen recognition proteins to go from being equally distributed on the white blood cell surface to being clustered at the point of contact?
- A 65-year-old man who has been living for years with debilitating hepatitis C finally receives a liver transplant. Tragically, a week into his recovery he contracts Pseudomonas aeruginosa enterocolitis that develops into lethal sepsis. According to the model below, these events could reasonably be explained by which? Quorum sensing Cross-species effects Microbial products affecting the host Butyrate Indole Others Host products affecting the microbiota Hormones Intestinal epithelial cells Choose one: O A. overgrowth of otherwise commensal flora B. increased activity of methanogens O C. development of antibiotic resistance D. surgery-induced stress O E. change in normal diet to hospital foodPathogen A has an ID50 of 10 cells and an LD50 of 10,000,000 cells. Pathogen B has an ID50 of 10,000 cells and an LD50 of 20,000 cells. From this information, we can determine that: ○ Pathogen A has higher infectivity but lower virulence than Pathogen B. ○ Pathogen A has lower infectivity but higher virulence than Pathogen B. ○ Pathogen B has higher infectivity but lower virulence than Pathogen A. ○ Pathogen B has higher infectivity and higher virulence than Pathogen A.Before development of a vaccine against this microbe, thedisease it caused accounted for two-thirds of bacterial meningi-tis cases during the first year of life but is still the number oneleading cause of mental retardation in patients who survive seri-ous disease due to permanent central nervous system disorders.What is the microorganism?(a) Haemophilus influenzae type B(b) Haemophilus influenzae type A(c) Neisseria meningitidis(d) Streptococcus pneumoniae(e) Listeria monocytogenes
- Chagas disease, also known as American trypanosomiasis, is a tropical parasiticdisease caused by Trypanosoma cruzi. It is spread mostly by insects known as Triatominae, or "kissing bugs". The symptoms change over the course of the infection and can affect enteric neurons. Potential life-threatening complications result from all of the following except- O increased production of IL-10 loss of neurons lack of coordinated propulsive pattern in colon mediated by ENSPenicillin was first used in the 1940s to treat gonorrhea infections produced by the bacterium Neisseria gonorrhoeae. In 1984, according to the CDC, fewer than 1% of gonorrhea infections were caused by penicillin-resistant N. gonorrhoeae. By 1990, more than 10% of cases were penicillin resistant and a few years later the level of resistance was 95%. Explain the various ways this resistance could be spread among the cells. Could this resistance pass to other infectious bacteria from N. gonorrhoeae?The process by which point mutations cause slight changes in the spike proteins hemagglutinin and neuraminidase of the influenza virus is called antigenic shift tranformation transduction antigenic drift