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The process by which alteration in the genetic makeup of live type IIR bacteria was performed by heat killed type IIIS bacteria.
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- Explain the process by which alteration in the genetic makeup of live type IIR bacteria was performed by heat killed type IIIS bacteria.With some level of toxic shock syndrome caused by the superantigen produced by Staphylococcus aureus, why the antibiotics are not effective after a certain point, even though the pathogen is susceptible to them?Bacteria have a single circular chromosome while human cells have 46 linear chromosomes. This means bacteria are considered half lloyd having only one copy of each gene.
- Penicillin 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?Streptococcus pneumoniae is a Gram-positive bacterium that colonizes the mucosal surface of the upper respiratory tract in humans. The presence of this bacterium in the nose and throat is widespread in the population, and in most people, colonization with Strep. pneumoniae is asymptomatic. The figure attached shows a comparison of in vitro growth curves of the wild-type strain of Strep. pneumoniae, as well as a Strep. pneumoniae mutant strain with a defect in one bacterial gene. The graph on the right shows the growth curve following addition of lysozyme during the logarithmic phase of bacterial growth. Which statement could account for the data in these graphs? Strain B is wild-type Strep. pneumoniae, and strain A is a mutant that cannot modify its peptidoglycan to be lysozyme-resistant. Strain B is wild-type Strep. pneumoniae, and strain A is a mutant that that expresses increased levels of LPS. Strain A is wild-type Strep. pneumoniae, and strain B is a mutant that cannot modify its…A suspected pathogen is observed from the blood of a diseased mouse. An investigation of the other mice in the area indicates that it is not present in healthy mice. With Koch's postulates in mind, what is the next step to determine whether or not this suspected pathogen is the cause of disease in the mouse? a) Grow the suspected pathogen in a pure culture Ob) Re-isolate the suspected pathogen and show that it is the same as the original pathogen c) Inoculate a healthy mouse with the suspected pathogen O d) Determine whether the organism in the pure culture is the same one as in the original sample
- 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 monocytogenesWhich statement among A-D is false regarding bacterial toxins? A) O Hemolysıns are cell membrane disrupters that can rupture red blood cells. B) O Second mesengar pathway disrupters like cholera toxin produces a debilitating respiratory condition of the lungs. C) O Shiga toxin, tetanus toxin, and hemolysins are all types of exotoxins. D) O Superantigens elicit a hyperactive response by the immune system and can lead to shock. E) O None are false, A-D are all true statements.What is the relationship between the superantigens of S. aureus and the organism’s production of toxic shock?
- It was important for Lilly to understand how the bacteria were able to cause disease in patients. The mechanism of pathogenesis by M. tuberculosis starts in the lung alveoli. The cell wall of M. tuberculosis allows it to resist phagocytolysis by the alveolar macrophages, where they can multiply. They can then induce apoptosis in macrophages, which die, and the bacteria is free to infect other macrophages. As the cycle of infection slowly progresses, the body's response to the infection is to try to wall off the bacteria in granulomas (wall of immune cells, both dead and alive, surrounding the bacteria to restrict its spread). Eventually, the bacteria can escape the granuloma and infect other parts of the lung. Transmission of Mtb Initial infection and Granuloma cavitation replication of Mtb in macrophages and dissemination of Mtb in the lung Infected macrophages Caseating granuloma Recruitment of Innate and adaptive immune cells Infected cells undergo necrosis resulting in the…It was important for Lilly to understand how the bacteria were able to cause disease in patients. The mechanism of pathogenesis by M. tuberculosis starts in the lung alveoli. The cell wall of M. tuberculosis allows it to resist phagocytolysis by the alveolar macrophages, where they can multiply. They can then induce apoptosis in macrophages, which die, and the bacteria is free to infect other macrophages. As the cycle of infection slowly progresses, the body's response to the infection is to try to wall off the bacteria in granulomas (wall of immune cells, both dead and alive, surrounding the bacteria to restrict its spread). Eventually, the bacteria can escape the granuloma and infect other parts of the lung. Transmission of Mtb Initial infection and Granuloma cavitationy replication of Mtb in macrophages and dissemination of Mtb in the lung Infected macrophages Caseating granuloma Recruitment of Innate and adaptive immune cells Infected cells undergo necrosis resulting in the…Type S Streptococcus pneumoniae bacterium is lethal and will kill its host. If heat inactivated the S strain dies and becomes nonlethal. Type R Streptococcus pneumoniae is a nonvirulent strain of bacteria. What would occur if one were to inject both the R strain and heat-killed S strains into a host organism such as the mouse? The R strain would be transformed into the virulent S strain and kill the host. Neither the S nor the R strain would change. The R strain would be transformed into the virulent S strain and not affect the host. The S strain would be transformed into the nonvirulent R strain and not affect the host The S strain would be transformed into the nonvirulent R strain and kill the host.